A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.
A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.
A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.
Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.
Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.
Triglycerides are the most common type of fat in the body, stored in fat cells and used as energy; they are measured in blood tests to assess heart disease risk, with high levels often resulting from dietary habits, obesity, physical inactivity, smoking, and alcohol consumption.
Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.
A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.
Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.
Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.
A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.
A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.
Conditions with excess LIPIDS in the blood.
Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.
A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).
Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.
Cholesterol present in food, especially in animal products.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
A condition of elevated levels of TRIGLYCERIDES in the blood.
A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
Relating to the size of solids.
Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.
The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
Substances used to lower plasma CHOLESTEROL levels.
An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The rate dynamics in chemical or physical systems.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.
Transport proteins that carry specific substances in the blood or across cell membranes.
The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.
An inherited condition due to a deficiency of either LIPOPROTEIN LIPASE or APOLIPOPROTEIN C-II (a lipase-activating protein). The lack of lipase activities results in inability to remove CHYLOMICRONS and TRIGLYCERIDES from the blood which has a creamy top layer after standing.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.
A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
The main trunk of the systemic arteries.
A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.
A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.
Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.
A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).
A class of oxidized LDL receptors that contain LECTIN-like extracellular domains.
An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.
A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.
Electrophoresis in which agar or agarose gel is used as the diffusion medium.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.
An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.
Peroxides produced in the presence of a free radical by the oxidation of unsaturated fatty acids in the cell in the presence of molecular oxygen. The formation of lipid peroxides results in the destruction of the original lipid leading to the loss of integrity of the membranes. They therefore cause a variety of toxic effects in vivo and their formation is considered a pathological process in biological systems. Their formation can be inhibited by antioxidants, such as vitamin E, structural separation or low oxygen tension.
A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).
An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Elements of limited time intervals, contributing to particular results or situations.
Derivatives of PHOSPHATIDYLCHOLINES obtained by their partial hydrolysis which removes one of the fatty acid moieties.
Abstaining from all food.

Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, generates two bioactive products during the oxidation of low-density lipoprotein: use of a novel inhibitor. (1/6753)

A novel and potent azetidinone inhibitor of the lipoprotein-associated phospholipase A2 (Lp-PLA2), i.e. platelet-activating factor acetylhydrolase, is described for the first time. This inhibitor, SB-222657 (Ki=40+/-3 nM, kobs/[I]=6. 6x10(5) M-1.s-1), is inactive against paraoxonase, is a poor inhibitor of lecithin:cholesterol acyltransferase and has been used to investigate the role of Lp-PLA2 in the oxidative modification of lipoproteins. Although pretreatment with SB-222657 did not affect the kinetics of low-density lipoprotein (LDL) oxidation by Cu2+ or an azo free-radical generator as determined by assay of lipid hydroperoxides (LOOHs), conjugated dienes and thiobarbituric acid-reacting substances, in both cases it inhibited the elevation in lysophosphatidylcholine content. Moreover, the significantly increased monocyte chemoattractant activity found in a non-esterified fatty acid fraction from LDL oxidized by Cu2+ was also prevented by pretreatment with SB-222657, with an IC50 value of 5.0+/-0.4 nM. The less potent diastereoisomer of SB-222657, SB-223777 (Ki=6.3+/-0.5 microM, kobs/[I]=1.6x10(4) M-1.s-1), was found to be significantly less active in both assays. Thus, in addition to generating lysophosphatidylcholine, a known biologically active lipid, these results demonstrate that Lp-PLA2 is capable of generating oxidized non-esterified fatty acid moieties that are also bioactive. These findings are consistent with our proposal that Lp-PLA2 has a predominantly pro-inflammatory role in atherogenesis. Finally, similar studies have demonstrated that a different situation exists during the oxidation of high-density lipoprotein, with enzyme(s) other than Lp-PLA2 apparently being responsible for generating lysophosphatidylcholine.  (+info)

Antiphospholipid, anti-beta 2-glycoprotein-I and anti-oxidized-low-density-lipoprotein antibodies in antiphospholipid syndrome. (2/6753)

Antiphospholipid antibodies (aPL), anti-beta 2-glycoprotein I (anti-beta 2-GPI) and anti-oxidized-low-density lipoprotein (LDL) antibodies are all implicated in the pathogenesis of antiphospholipid syndrome. To investigate whether different autoantibodies or combinations thereof produced distinct effects related to their antigenic specificities, we examined the frequencies of antiphospholipid syndrome (APS)-related features in the presence of different antibodies [aPL, beta 2-GPI, anti-oxidized low density lipoprotein (LDL)] in 125 patients with APS. Median follow-up was 72 months: 58 patients were diagnosed as primary APS and 67 as APS plus systemic lupus erythematosus (SLE). Anticardiolipin antibodies (aCL), anti-beta 2-GPI and anti-oxidized LDL antibodies were determined by ELISA; lupus anticoagulant (LA) by standard coagulometric methods. Univariate analysis showed that patients positive for anti-beta 2-GPI had a higher risk of recurrent thrombotic events (OR = 3.64, 95% CI, p = 0.01) and pregnancy loss (OR = 2.99, 95% CI, p = 0.004). Patients positive for anti-oxidized LDL antibodies had a 2.24-fold increase in the risk of arterial thrombosis (2.24, 95% CI, p = 0.03) and lower risk of thrombocytopenia (OR = 0.41 95% CI, p = 0.04). Patients positive for aCL antibodies had a higher risk of pregnancy loss (OR = 4.62 95% CI, p = 0.001). When these data were tested by multivariate logistic regression, the association between anti-beta 2-GPI and pregnancy loss and the negative association between anti-oxidized LDL antibodies and thrombocytopenia disappeared.  (+info)

Suppression of atherosclerotic development in Watanabe heritable hyperlipidemic rabbits treated with an oral antiallergic drug, tranilast. (3/6753)

BACKGROUND: Inflammatory and immunological responses of vascular cells have been shown to play a significant role in the progression of atheromatous formation. Tranilast [N-(3,4-dimethoxycinnamoyl) anthranillic acid] inhibits release of cytokines and chemical mediators from various cells, including macrophages, leading to suppression of inflammatory and immunological responses. This study tested whether tranilast may suppress atheromatous formation in Watanabe heritable hyperlipidemic (WHHL) rabbits. METHODS AND RESULTS: WHHL rabbits (2 months old) were given either 300 mg x kg-1 x d-1 of tranilast (Tranilast, n=12) or vehicle (Control, n=13) PO for 6 months. Tranilast treatment was found to suppress the aortic area covered with plaque. Immunohistochemical analysis showed that there was no difference in the percentage of the RAM11-positive macrophage area and the frequency of CD5-positive cells (T cells) in intimal plaques between Tranilast and Control. Major histocompatibility complex (MHC) class II expression in macrophages and interleukin-2 (IL-2) receptor expression in T cells, as markers of the immunological activation in these cells, was suppressed in atheromatous plaque by tranilast treatment. Flow cytometry analysis of isolated human and rabbit peripheral blood mononuclear cells showed that an increase in expression both of MHC class II antigen on monocytes by incubation with interferon-gamma and of IL-2 receptor on T cells by IL-2 was suppressed by the combined incubation with tranilast. CONCLUSIONS: The results indicate that tranilast suppresses atherosclerotic development partly through direct inhibition of immunological activation of monocytes/macrophages and T cells in the atheromatous plaque.  (+info)

Hypoalbuminemia increases lysophosphatidylcholine in low-density lipoprotein of normocholesterolemic subjects. (4/6753)

BACKGROUND: A phospholipid, lysophosphatidylcholine (LPC), is the major determinant of the atherosclerotic properties of oxidized low-density lipoprotein (LDL). Under normal circumstances most LPC is bound to albumin. We hypothesized that lipoprotein LPC concentrations are increased in hypoalbuminemic patients with the nephrotic syndrome, irrespective of their lipid levels. To test this hypothesis, we selected nephrotic and control subjects with matched LDL cholesterol levels. METHODS: Lipoproteins and the albumin-rich lipoprotein-deficient fractions were separated by ultracentrifugation and their phospholipid composition was analyzed by thin-layer chromatography. RESULTS: Nephrotic subjects (albumin 23 +/- 2 g/liter and LDL cholesterol 3.1 +/- 0.2 mmol/liter) had a LDL LPC concentration that was increased (P < 0.05) to 66 +/- 7 vs. 35 +/- 6 micromol/liter in matched controls (albumin 42 +/- 5 g/liter and LDL cholesterol 3.1 +/- 0.2 mmol/liter). LPC in very low-density lipoprotein plus intermediate-density lipoprotein (VLDL + IDL) in these subjects was also increased to 33 +/- 7 vs. 9 +/- 2 micromol/liter in controls (P < 0.05). Conversely, LPC was decreased to 19 +/- 4 micromol/liter in the albumin-containing fraction of these hypoalbuminemic patients, as compared to 46 +/- 10 micromol/liter in the controls (P < 0.05). LPC was also low (14 +/- 4 micromol/liter) in the albumin-containing fraction of hypoalbuminemic, hypocholesterolemic patients with nonrenal diseases. In hyperlipidemic nephrotic subjects (albumin 21 +/- 2 g/liter and LDL cholesterol 5.7 +/- 0.5 mmol/liter) the LPC levels in LDL and VLDL + IDL were further increased, to 95 +/- 20 and 56 +/- 23 micromol/liter, respectively (P < 0.05). CONCLUSION: These findings suggest that in the presence of hypoalbuminemia in combination with proteinuria, LPC shifts from albumin to VLDL, IDL and LDL. This effect is independent of hyperlipidemia. Increased LPC in lipoproteins may be an important factor in the disproportionate increase in cardiovascular disease in nephrotic patients with hypoalbuminemia.  (+info)

Liver-specific inactivation of the abetalipoproteinemia gene completely abrogates very low density lipoprotein/low density lipoprotein production in a viable conditional knockout mouse. (5/6753)

Conventional knockout of the microsomal triglyceride transfer protein large subunit (lMTP) gene is embryonic lethal in the homozygous state in mice. We have produced a conditional lMTP knockout mouse by inserting loxP sequences flanking exons 5 and 6 by gene targeting. Homozygous floxed mice were born live with normal plasma lipids. Intravenous injection of an adenovirus harboring Cre recombinase (AdCre1) produced deletion of exons 5 and 6 and disappearance of lMTP mRNA and immunoreactive protein in a liver-specific manner. There was also disappearance of plasma apolipoprotein (apo) B-100 and marked reduction in apoB-48 levels. Wild-type mice showed no response, and heterozygous mice, an intermediate response, to AdCre1. Wild-type mice doubled their plasma cholesterol level following a high cholesterol diet. This hypercholesterolemia was abolished in AdCre1-treated lMTP-/- mice, the result of a complete absence of very low/intermediate/low density lipoproteins and a slight reduction in high density lipoprotein. Heterozygous mice showed an intermediate lipoprotein phenotype. The rate of accumulation of plasma triglyceride following Triton WR1339 treatment in lMTP-/- mice was <10% that in wild-type animals, indicating a failure of triglyceride-rich lipoprotein production. Pulse-chase experiments using hepatocytes isolated from wild-type and lMTP-/- mice revealed a failure of apoB secretion in lMTP-/- animals. Therefore, the liver-specific inactivation of the lMTP gene completely abrogates apoB-100 and very low/intermediate/low density lipoprotein production. These conditional knockout mice are a useful in vivo model for studying the role of MTP in apoB biosynthesis and the biogenesis of apoB-containing lipoproteins.  (+info)

Platelet high affinity low density lipoprotein binding and import of lipoprotein derived phospholipids. (6/6753)

The binding of low density lipoprotein (LDL) to the platelet cell membrane could facilitate the transfer of phospholipids from LDL to the platelets. A polyclonal antibody against the platelet glycoproteins IIb/IIIa inhibited the high affinity binding of 125I-LDL by up to 80%. The transfer of pyrene (py)-labeled sphingomyelin (SM), phosphatidylcholine and phosphatidylethanolamine from LDL to the platelets was unaffected by the antibody. The lectin wheat germ agglutinin (WGA) reduced the binding of 125I-LDL to the platelets by approximately 80%. In contrast, the lectin stimulated the transfer of SM from LDL into the platelets by about three-fold. WGA also specifically augmented the transfer of py-SM between lipid vesicles and the platelets, the stimulation being abolished in the presence of N-acetylglucosamine. Dextran sulfate (DS) increased the specific binding of 125I-LDL to the platelets by up to 2.8-fold. On the other hand, the import of LDL-derived py-phospholipids was unaffected by DS. Together, the results indicate that the phospholipid transfer from LDL to the platelets is independent of the high affinity LDL binding to the platelets and is specifically stimulated by WGA. Thus, the interactions of platelets with LDL phospholipids differ markedly from those with the apoprotein components of the lipoproteins.  (+info)

Oxidized low-density lipoprotein regulates matrix metalloproteinase-9 and its tissue inhibitor in human monocyte-derived macrophages. (7/6753)

BACKGROUND: Macrophages in human atherosclerotic plaques produce a family of matrix metalloproteinases (MMPs), which may influence vascular remodeling and plaque disruption. Because oxidized LDL (ox-LDL) is implicated in many proatherogenic events, we hypothesized that ox-LDL would regulate expression of MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in monocyte-derived macrophages. MWRHOSA AND RESULTS: Mononuclear cells were isolated from normal human subjects with Ficoll-Paque density gradient centrifugation, and adherent cells were allowed to differentiate into macrophages during 7 days of culture in plastic dishes. On day 7, by use of serum-free medium, the macrophages were incubated with various concentrations of native LDL (n-LDL) and copper-oxidized LDL. Exposure to ox-LDL (10 to 50 microg/mL) increased MMP-9 mRNA expression as analyzed by Northern blot, protein expression as measured by ELISA and Western blot, and gelatinolytic activity as determined by zymography. The increase in MMP-9 expression was associated with increased nuclear binding of transcription factor NF-kappaB and AP-1 complex on electromobility shift assay. In contrast, ox-LDL (10 to 50 microg/mL) decreased TIMP-1 expression. Ox-LDL-induced increase in MMP-9 expression was abrogated by HDL (100 microg/mL). n-LDL had no significant effect on MMP-9 or TIMP-1 expression. CONCLUSIONS: These data demonstrate that unlike n-LDL, ox-LDL upregulates MMP-9 expression while reducing TIMP-1 expression in monocyte-derived macrophages. Furthermore, HDL abrogates ox-LDL-induced MMP-9 expression. Thus, ox-LDL may contribute to macrophage-mediated matrix breakdown in the atherosclerotic plaques, thereby predisposing them to plaque disruption and/or vascular remodeling.  (+info)

Antibodies against phospholipids and oxidized LDL in alcoholic patients. (8/6753)

Antiphospholipid antibodies (APA) are a generic term describing antibodies that recognize various phospholipids. Hepatocyte damage is a cardinal event in the course of alcoholic liver injury and autoantibodies against phospholipids could play an important role in this process. APA in alcoholic patients seem to reflect membrane lesions, impairment of immunological reactivity, liver disease progression and they correlate significantly with disease severity. LDL oxidation is supposed to be one of the most important pathogenic mechanisms of atherosclerosis and antibodies against oxidized low-density lipoprotein (oxLDL) are some kind of an epiphenomenon of this process. The scope of our study was to determine some autoantibodies (IgG-oxLDL and antiphospholipid antibodies) and their possible changes in alcoholic patients. We studied IgG-oxLDL and four APA - anticardiolipin antibodies (ACA), antiphosphatidylserine antibodies (APSA) antiphosphatidylethanolamine antibodies (APE) and antiphosphatidylcholine antibodies (APCA) in 35 alcoholic patients with mildly affected liver function at the beginning of the abuse treatment. The control group consisted of 60 healthy blood donors. In the studied group, we obtained positive results concerning total ACA in 17.1 % of alcoholic patients (8.3 % in the control group), 11.4 % IgG-ACA (6.7 %), 8.6 % IgM-ACA (3.3 %), 14.3 % total APE (6.7 %), 14.3 % total APCA (8.3 %) and 20 % total APSA (8.3 % in the control group). The IgG-oxLDL (406.4+/-52.5 vs 499.9+/-52.5 mU/ml) was not affected in alcoholic patients. We conclude that the autoantibodies against oxLDL are present in sera of alcoholics and healthy blood donors. Based on our results which revealed a wide range of IgG-oxLDL titres in the healthy population, this parameter does not appear to be very promising for the evaluation of the risk of atherosclerosis. Alcoholics with only mild affection of liver functions did not exhibit a significantly higher prevalence of all studied antiphospholipid antibodies (ACA, APSA, APE, APCA) which could lead to membrane lesions in these patients.  (+info)

Low-density lipoproteins (LDL), also known as "bad cholesterol," are a type of lipoprotein that carry cholesterol and other fats from the liver to cells throughout the body. High levels of LDL in the blood can lead to the buildup of cholesterol in the walls of the arteries, which can increase the risk of heart disease and stroke.

Lipoproteins are complex particles composed of proteins (apolipoproteins) and lipids (cholesterol, triglycerides, and phospholipids) that are responsible for transporting fat molecules around the body in the bloodstream. LDL is one type of lipoprotein, along with high-density lipoproteins (HDL), very low-density lipoproteins (VLDL), and chylomicrons.

LDL particles are smaller than HDL particles and can easily penetrate the artery walls, leading to the formation of plaques that can narrow or block the arteries. Therefore, maintaining healthy levels of LDL in the blood is essential for preventing cardiovascular disease.

Lipoproteins are complex particles composed of multiple proteins and lipids (fats) that play a crucial role in the transport and metabolism of fat molecules in the body. They consist of an outer shell of phospholipids, free cholesterols, and apolipoproteins, enclosing a core of triglycerides and cholesteryl esters.

There are several types of lipoproteins, including:

1. Chylomicrons: These are the largest lipoproteins and are responsible for transporting dietary lipids from the intestines to other parts of the body.
2. Very-low-density lipoproteins (VLDL): Produced by the liver, VLDL particles carry triglycerides to peripheral tissues for energy storage or use.
3. Low-density lipoproteins (LDL): Often referred to as "bad cholesterol," LDL particles transport cholesterol from the liver to cells throughout the body. High levels of LDL in the blood can lead to plaque buildup in artery walls and increase the risk of heart disease.
4. High-density lipoproteins (HDL): Known as "good cholesterol," HDL particles help remove excess cholesterol from cells and transport it back to the liver for excretion or recycling. Higher levels of HDL are associated with a lower risk of heart disease.

Understanding lipoproteins and their roles in the body is essential for assessing cardiovascular health and managing risks related to heart disease and stroke.

High-Density Lipoproteins (HDL) are a type of lipoprotein that play a crucial role in the transportation and metabolism of cholesterol in the body. They are often referred to as "good" cholesterol because they help remove excess cholesterol from cells and carry it back to the liver, where it can be broken down and removed from the body. This process is known as reverse cholesterol transport.

HDLs are composed of a lipid core containing cholesteryl esters and triglycerides, surrounded by a shell of phospholipids, free cholesterol, and apolipoproteins, primarily apoA-I. The size and composition of HDL particles can vary, leading to the classification of different subclasses of HDL with varying functions and metabolic fates.

Elevated levels of HDL have been associated with a lower risk of developing cardiovascular diseases, while low HDL levels increase the risk. However, it is essential to consider that HDL function and quality may be more important than just the quantity in determining cardiovascular risk.

VLDL (Very Low-Density Lipoproteins) are a type of lipoprotein that play a crucial role in the transport and metabolism of fat molecules, known as triglycerides, in the body. They are produced by the liver and consist of a core of triglycerides surrounded by a shell of proteins called apolipoproteins, phospholipids, and cholesterol.

VLDL particles are responsible for delivering fat molecules from the liver to peripheral tissues throughout the body, where they can be used as an energy source or stored for later use. During this process, VLDL particles lose triglycerides and acquire more cholesterol, transforming into intermediate-density lipoproteins (IDL) and eventually low-density lipoproteins (LDL), which are also known as "bad" cholesterol.

Elevated levels of VLDL in the blood can contribute to the development of cardiovascular disease due to their association with increased levels of triglycerides and LDL cholesterol, as well as decreased levels of high-density lipoproteins (HDL), which are considered "good" cholesterol.

LDL receptors (Low-Density Lipoprotein Receptors) are cell surface receptors that play a crucial role in the regulation of cholesterol homeostasis within the body. They are responsible for recognizing and binding to LDL particles, also known as "bad cholesterol," which are then internalized by the cell through endocytosis.

Once inside the cell, the LDL particles are broken down, releasing their cholesterol content, which can be used for various cellular processes such as membrane synthesis and hormone production. The LDL receptors themselves are recycled back to the cell surface, allowing for continued uptake of LDL particles.

Mutations in the LDL receptor gene can lead to a condition called familial hypercholesterolemia, which is characterized by high levels of LDL cholesterol in the blood and an increased risk of premature cardiovascular disease.

Lipoprotein lipase (LPL) is an enzyme that plays a crucial role in the metabolism of lipids. It is responsible for breaking down triglycerides, which are the main constituent of dietary fats and chylomicrons, into fatty acids and glycerol. These products are then taken up by cells for energy production or storage.

LPL is synthesized in various tissues, including muscle and fat, where it is attached to the inner lining of blood vessels (endothelium). The enzyme is activated when it comes into contact with lipoprotein particles, such as chylomicrons and very-low-density lipoproteins (VLDL), which transport triglycerides in the bloodstream.

Deficiencies or mutations in LPL can lead to various metabolic disorders, including hypertriglyceridemia, a condition characterized by high levels of triglycerides in the blood. Conversely, overexpression of LPL has been associated with increased risk of atherosclerosis due to excessive uptake of fatty acids by macrophages and their conversion into foam cells, which contribute to plaque formation in the arteries.

LDL, or low-density lipoprotein, is often referred to as "bad" cholesterol. It is one of the lipoproteins that helps carry cholesterol throughout your body. High levels of LDL cholesterol can lead to a buildup of cholesterol in your arteries, which can increase the risk of heart disease and stroke.

Cholesterol is a type of fat (lipid) that is found in the cells of your body. Your body needs some cholesterol to function properly, but having too much can lead to health problems. LDL cholesterol is one of the two main types of cholesterol; the other is high-density lipoprotein (HDL), or "good" cholesterol.

It's important to keep your LDL cholesterol levels in a healthy range to reduce your risk of developing heart disease and stroke. A healthcare professional can help you determine what your target LDL cholesterol level should be based on your individual health status and risk factors.

Cholesterol is a type of lipid (fat) molecule that is an essential component of cell membranes and is also used to make certain hormones and vitamins in the body. It is produced by the liver and is also obtained from animal-derived foods such as meat, dairy products, and eggs.

Cholesterol does not mix with blood, so it is transported through the bloodstream by lipoproteins, which are particles made up of both lipids and proteins. There are two main types of lipoproteins that carry cholesterol: low-density lipoproteins (LDL), also known as "bad" cholesterol, and high-density lipoproteins (HDL), also known as "good" cholesterol.

High levels of LDL cholesterol in the blood can lead to a buildup of cholesterol in the walls of the arteries, increasing the risk of heart disease and stroke. On the other hand, high levels of HDL cholesterol are associated with a lower risk of these conditions because HDL helps remove LDL cholesterol from the bloodstream and transport it back to the liver for disposal.

It is important to maintain healthy levels of cholesterol through a balanced diet, regular exercise, and sometimes medication if necessary. Regular screening is also recommended to monitor cholesterol levels and prevent health complications.

Apolipoprotein B (ApoB) is a type of protein that plays a crucial role in the metabolism of lipids, particularly low-density lipoprotein (LDL) or "bad" cholesterol. ApoB is a component of LDL particles and serves as a ligand for the LDL receptor, which is responsible for the clearance of LDL from the bloodstream.

There are two main forms of ApoB: ApoB-100 and ApoB-48. ApoB-100 is found in LDL particles, very low-density lipoprotein (VLDL) particles, and chylomicrons, while ApoB-48 is only found in chylomicrons, which are produced in the intestines and responsible for transporting dietary lipids.

Elevated levels of ApoB are associated with an increased risk of cardiovascular disease (CVD), as they indicate a higher concentration of LDL particles in the bloodstream. Therefore, measuring ApoB levels can provide additional information about CVD risk beyond traditional lipid profile tests that only measure total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.

Lipoprotein receptors are specialized proteins found on the surface of cells that play a crucial role in the metabolism of lipoproteins, which are complex particles composed of lipids and proteins. These receptors bind to specific lipoproteins in the bloodstream, facilitating their uptake into the cell for further processing.

There are several types of lipoprotein receptors, including:

1. LDL (Low-Density Lipoprotein) Receptor: This receptor is responsible for recognizing and internalizing LDL particles, which are rich in cholesterol. Once inside the cell, LDL particles release their cholesterol, which can then be used for various cellular functions or stored for later use. Defects in the LDL receptor can lead to elevated levels of LDL cholesterol in the blood and an increased risk of developing cardiovascular disease.
2. HDL (High-Density Lipoprotein) Receptor: This receptor is involved in the clearance of HDL particles from the bloodstream. HDL particles are responsible for transporting excess cholesterol from peripheral tissues to the liver, where it can be processed and eliminated from the body.
3. VLDL (Very Low-Density Lipoprotein) Receptor: This receptor recognizes and internalizes VLDL particles, which are produced by the liver and carry triglycerides and cholesterol to peripheral tissues. VLDL particles are subsequently converted into LDL particles in the bloodstream.
4. LRP (Low-Density Lipoprotein Receptor-Related Protein) Family: This family of receptors includes several members, such as LRP1 and LRP2, that play roles in various cellular processes, including lipid metabolism, protein trafficking, and cell signaling. They can bind to a variety of ligands, including lipoproteins, proteases, and extracellular matrix components.

In summary, lipoprotein receptors are essential for maintaining proper lipid metabolism and homeostasis by facilitating the uptake, processing, and elimination of lipoproteins in the body.

Triglycerides are the most common type of fat in the body, and they're found in the food we eat. They're carried in the bloodstream to provide energy to the cells in our body. High levels of triglycerides in the blood can increase the risk of heart disease, especially in combination with other risk factors such as high LDL (bad) cholesterol, low HDL (good) cholesterol, and high blood pressure.

It's important to note that while triglycerides are a type of fat, they should not be confused with cholesterol, which is a waxy substance found in the cells of our body. Both triglycerides and cholesterol are important for maintaining good health, but high levels of either can increase the risk of heart disease.

Triglyceride levels are measured through a blood test called a lipid panel or lipid profile. A normal triglyceride level is less than 150 mg/dL. Borderline-high levels range from 150 to 199 mg/dL, high levels range from 200 to 499 mg/dL, and very high levels are 500 mg/dL or higher.

Elevated triglycerides can be caused by various factors such as obesity, physical inactivity, excessive alcohol consumption, smoking, and certain medical conditions like diabetes, hypothyroidism, and kidney disease. Medications such as beta-blockers, steroids, and diuretics can also raise triglyceride levels.

Lifestyle changes such as losing weight, exercising regularly, eating a healthy diet low in saturated and trans fats, avoiding excessive alcohol consumption, and quitting smoking can help lower triglyceride levels. In some cases, medication may be necessary to reduce triglycerides to recommended levels.

Apolipoproteins are a group of proteins that are associated with lipids (fats) in the body and play a crucial role in the metabolism, transportation, and regulation of lipids. They are structural components of lipoprotein particles, which are complexes of lipids and proteins that transport lipids in the bloodstream.

There are several types of apolipoproteins, including ApoA, ApoB, ApoC, ApoD, ApoE, and others. Each type has a specific function in lipid metabolism. For example, ApoA is a major component of high-density lipoprotein (HDL), often referred to as "good cholesterol," and helps remove excess cholesterol from cells and tissues and transport it to the liver for excretion. ApoB, on the other hand, is a major component of low-density lipoprotein (LDL), or "bad cholesterol," and plays a role in the delivery of cholesterol to cells and tissues.

Abnormal levels of apolipoproteins or dysfunctional forms of these proteins have been linked to various diseases, including cardiovascular disease, Alzheimer's disease, and metabolic disorders such as diabetes. Therefore, measuring apolipoprotein levels in the blood can provide valuable information for diagnosing and monitoring these conditions.

IDL, or intermediate-density lipoproteins, are a type of lipoprotein that is denser than low-density lipoproteins (LDL) but less dense than high-density lipoproteins (HDL). They are formed during the catabolism (breakdown) of VLDL (very low-density lipoproteins), another type of lipoprotein, by lipoprotein lipase, an enzyme that breaks down triglycerides in lipoproteins.

IDLs contain a higher proportion of cholesterol and apolipoprotein E (apoE) compared to VLDLs and LDLs. Some IDLs are taken up by the liver, while others are converted into LDL particles through the action of cholesteryl ester transfer protein (CETP), which exchanges triglycerides in LDL for cholesterol esters in IDL.

Elevated levels of IDLs in the blood may be a risk factor for cardiovascular disease, as they can contribute to the formation and accumulation of plaque in the arteries. However, IDLs are not typically measured in routine clinical testing, and their role in disease is not as well understood as that of LDL or HDL.

HDL3 (High-Density Lipoprotein 3) is a type of lipoprotein that plays a role in the transport and metabolism of cholesterol in the body. HDLs are commonly known as "good cholesterol" because they help remove excess cholesterol from cells and carry it back to the liver, where it can be broken down and removed from the body.

HDL3 is one of the subclasses of HDL based on its density and size. It is denser than HDL2 but less dense than HDL1. HDL3 is smaller in size and contains a higher proportion of protein to lipid compared to other HDL subclasses. It is also more efficient in reverse cholesterol transport, which is the process of removing cholesterol from tissues and delivering it to the liver for excretion.

It's worth noting that while high levels of HDL are generally associated with a lower risk of heart disease, recent research suggests that the relationship between HDL and cardiovascular health may be more complex than previously thought.

HDL (High-Density Lipoprotein) cholesterol is often referred to as "good" cholesterol. It is a type of lipoprotein that helps remove excess cholesterol from cells and carry it back to the liver, where it can be broken down and removed from the body. High levels of HDL cholesterol have been associated with a lower risk of heart disease and stroke.

Lipids are a broad group of organic compounds that are insoluble in water but soluble in nonpolar organic solvents. They include fats, waxes, sterols, fat-soluble vitamins (such as vitamins A, D, E, and K), monoglycerides, diglycerides, triglycerides, and phospholipids. Lipids serve many important functions in the body, including energy storage, acting as structural components of cell membranes, and serving as signaling molecules. High levels of certain lipids, particularly cholesterol and triglycerides, in the blood are associated with an increased risk of cardiovascular disease.

HDL2 (High-Density Lipoprotein 2) is a type of lipoprotein that plays a role in the transportation and metabolism of cholesterol in the body. HDL particles are responsible for picking up excess cholesterol from tissues and cells throughout the body and transporting it back to the liver, where it can be broken down and removed from the body. This process is known as reverse cholesterol transport.

HDL2 is one of the subclasses of HDL particles, which are classified based on their size, density, and composition. HDL2 particles are larger and denser than other HDL subclasses, such as HDL3. They have a higher proportion of cholesteryl esters to phospholipids and apolipoproteins compared to other HDL subclasses.

Elevated levels of HDL2 have been associated with a lower risk of cardiovascular disease, while low levels of HDL2 have been linked to an increased risk of heart disease. However, the exact role of HDL2 in cardiovascular health and disease is still being studied and understood.

Cholesteryl esters are formed when cholesterol, a type of lipid (fat) that is important for the normal functioning of the body, becomes combined with fatty acids through a process called esterification. This results in a compound that is more hydrophobic (water-repelling) than cholesterol itself, which allows it to be stored more efficiently in the body.

Cholesteryl esters are found naturally in foods such as animal fats and oils, and they are also produced by the liver and other cells in the body. They play an important role in the structure and function of cell membranes, and they are also precursors to the synthesis of steroid hormones, bile acids, and vitamin D.

However, high levels of cholesteryl esters in the blood can contribute to the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries, which can increase the risk of heart disease and stroke. Cholesteryl esters are typically measured as part of a lipid profile, along with other markers such as total cholesterol, HDL cholesterol, and triglycerides.

Apolipoprotein E (ApoE) is a protein involved in the metabolism of lipids, particularly cholesterol. It is produced primarily by the liver and is a component of several types of lipoproteins, including very low-density lipoproteins (VLDL) and high-density lipoproteins (HDL).

ApoE plays a crucial role in the transport and uptake of lipids in the body. It binds to specific receptors on cell surfaces, facilitating the delivery of lipids to cells for energy metabolism or storage. ApoE also helps to clear cholesterol from the bloodstream and is involved in the repair and maintenance of tissues.

There are three major isoforms of ApoE, designated ApoE2, ApoE3, and ApoE4, which differ from each other by only a few amino acids. These genetic variations can have significant effects on an individual's risk for developing certain diseases, particularly cardiovascular disease and Alzheimer's disease. For example, individuals who inherit the ApoE4 allele have an increased risk of developing Alzheimer's disease, while those with the ApoE2 allele may have a reduced risk.

In summary, Apolipoprotein E is a protein involved in lipid metabolism and transport, and genetic variations in this protein can influence an individual's risk for certain diseases.

Apolipoprotein B-100 (apoB-100) is a large protein component of low-density lipoprotein (LDL), also known as "bad cholesterol." It plays a crucial role in the metabolism and transport of fats and cholesterol in the body. ApoB-100 is responsible for the binding of LDL to specific receptors on cell surfaces, facilitating the uptake of lipoprotein particles by cells. Elevated levels of apoB-100 in the blood are associated with an increased risk of developing cardiovascular diseases, such as atherosclerosis and coronary artery disease.

Chylomicrons are a type of lipoprotein that are responsible for carrying dietary lipids, such as triglycerides and cholesterol, from the intestines to other parts of the body through the lymphatic system and bloodstream. They are the largest lipoproteins and are composed of an outer layer of phospholipids, free cholesterol, and apolipoproteins, which surrounds a core of triglycerides and cholesteryl esters. Chylomicrons are produced in the intestinal mucosa after a meal containing fat, and their production is stimulated by the hormone cholecystokinin. Once in the bloodstream, chylomicrons interact with other lipoproteins and enzymes to deliver their lipid cargo to various tissues, including muscle and adipose tissue, where they are used for energy or stored for later use.

Low-Density Lipoprotein Receptor-Related Protein 1 (LRP1) is a large transmembrane receptor protein that belongs to the low-density lipoprotein receptor family. It plays a crucial role in various biological processes, including cellular signaling, endocytosis, and intracellular trafficking of ligands. LRP1 is widely expressed in many tissues, particularly in the brain, liver, and vascular endothelial cells.

LRP1 interacts with a diverse array of ligands, such as extracellular matrix proteins, apolipoproteins, proteinases, proteinase inhibitors, and various pathogen-associated molecules. The receptor is involved in the clearance of these ligands from the extracellular space through endocytosis, followed by intracellular degradation or recycling.

In the context of lipid metabolism, LRP1 has been implicated in the cellular uptake and degradation of Apolipoprotein E (ApoE)-containing lipoproteins, which are involved in the reverse transport of cholesterol from peripheral tissues to the liver. Dysregulation of LRP1 function has been linked to several diseases, including atherosclerosis, Alzheimer's disease, and various neurological disorders.

In summary, Low-Density Lipoprotein Receptor-Related Protein 1 (LRP1) is a multifunctional transmembrane receptor that plays essential roles in cellular signaling, endocytosis, and intracellular trafficking of various ligands. Its dysfunction has been implicated in several diseases related to lipid metabolism, neurodegeneration, and neurological disorders.

Arteriosclerosis is a general term that describes the hardening and stiffening of the artery walls. It's a progressive condition that can occur as a result of aging, or it may be associated with certain risk factors such as high blood pressure, high cholesterol, diabetes, smoking, and a sedentary lifestyle.

The process of arteriosclerosis involves the buildup of plaque, made up of fat, cholesterol, calcium, and other substances, in the inner lining of the artery walls. Over time, this buildup can cause the artery walls to thicken and harden, reducing the flow of oxygen-rich blood to the body's organs and tissues.

Arteriosclerosis can affect any of the body's arteries, but it is most commonly found in the coronary arteries that supply blood to the heart, the cerebral arteries that supply blood to the brain, and the peripheral arteries that supply blood to the limbs. When arteriosclerosis affects the coronary arteries, it can lead to heart disease, angina, or heart attack. When it affects the cerebral arteries, it can lead to stroke or transient ischemic attack (TIA). When it affects the peripheral arteries, it can cause pain, numbness, or weakness in the limbs, and in severe cases, gangrene and amputation.

Hyperlipidemias are a group of disorders characterized by an excess of lipids (fats) or lipoproteins in the blood. These include elevated levels of cholesterol, triglycerides, or both. Hyperlipidemias can be inherited (primary) or caused by other medical conditions (secondary). They are a significant risk factor for developing cardiovascular diseases, such as atherosclerosis and coronary artery disease.

There are two main types of lipids that are commonly measured in the blood: low-density lipoprotein (LDL) cholesterol, often referred to as "bad" cholesterol, and high-density lipoprotein (HDL) cholesterol, known as "good" cholesterol. High levels of LDL cholesterol can lead to the formation of plaques in the arteries, which can narrow or block them and increase the risk of heart attack or stroke. On the other hand, high levels of HDL cholesterol are protective because they help remove LDL cholesterol from the bloodstream.

Triglycerides are another type of lipid that can be measured in the blood. Elevated triglyceride levels can also contribute to the development of cardiovascular disease, particularly when combined with high LDL cholesterol and low HDL cholesterol levels.

Hyperlipidemias are typically diagnosed through a blood test that measures the levels of various lipids and lipoproteins in the blood. Treatment may include lifestyle changes, such as following a healthy diet, getting regular exercise, losing weight, and quitting smoking, as well as medication to lower lipid levels if necessary.

Apolipoprotein A (apoA) is a type of apolipoprotein that is primarily associated with high-density lipoproteins (HDL), often referred to as "good cholesterol." There are several subtypes of apoA, including apoA-I, apoA-II, and apoA-IV.

ApoA-I is the major protein component of HDL particles and plays a crucial role in reverse cholesterol transport, which is the process by which excess cholesterol is removed from tissues and delivered to the liver for excretion. Low levels of apoA-I have been linked to an increased risk of cardiovascular disease.

ApoA-II is another protein component of HDL particles, although its function is less well understood than that of apoA-I. Some studies suggest that apoA-II may play a role in regulating the metabolism of HDL particles.

ApoA-IV is found in both HDL and chylomicrons, which are lipoprotein particles that transport dietary lipids from the intestine to the liver. The function of apoA-IV is not well understood, but it may play a role in regulating appetite and energy metabolism.

Overall, apolipoproteins A are important components of HDL particles and play a critical role in maintaining healthy lipid metabolism and reducing the risk of cardiovascular disease.

Hypercholesterolemia is a medical term that describes a condition characterized by high levels of cholesterol in the blood. Specifically, it refers to an abnormally elevated level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, which can contribute to the development of fatty deposits in the arteries called plaques. Over time, these plaques can narrow and harden the arteries, leading to atherosclerosis, a condition that increases the risk of heart disease, stroke, and other cardiovascular complications.

Hypercholesterolemia can be caused by various factors, including genetics, lifestyle choices, and underlying medical conditions. In some cases, it may not cause any symptoms until serious complications arise. Therefore, regular cholesterol screening is essential for early detection and management of hypercholesterolemia. Treatment typically involves lifestyle modifications, such as a healthy diet, regular exercise, and weight management, along with medication if necessary.

VLDL, or very low-density lipoproteins, are a type of lipoprotein that carries triglycerides and cholesterol from the liver to other parts of the body. Cholesterol is a fatty substance found in the blood, and VLDL contains both triglycerides and cholesterol.

Cholesterol itself cannot dissolve in the blood and needs to be transported around the body by lipoproteins, which are protein molecules that encapsulate and carry fat molecules, such as cholesterol and triglycerides, through the bloodstream. VLDL is one of several types of lipoproteins, including low-density lipoproteins (LDL) and high-density lipoproteins (HDL).

Elevated levels of VLDL in the blood can contribute to the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries, which can increase the risk of heart disease and stroke. Therefore, maintaining healthy levels of VLDL and other lipoproteins is an important part of overall cardiovascular health.

Hyperlipoproteinemia Type II, also known as Fredrickson Type II or Familial Combined Hyperlipidemia, is a genetic disorder characterized by elevated levels of low-density lipoprotein (LDL) cholesterol and/or triglycerides in the blood. This condition can lead to an increased risk of developing cardiovascular diseases such as atherosclerosis and coronary artery disease.

The disorder is caused by mutations in several genes involved in lipid metabolism, including APOB, LDLR, PCSK9, and APOE. These genetic defects result in impaired clearance of LDL particles from the bloodstream, leading to their accumulation and increased risk of cardiovascular disease.

Individuals with Hyperlipoproteinemia Type II typically have elevated levels of both LDL cholesterol and triglycerides, although some may only have one or the other elevated. The disorder can present at any age, but it is often diagnosed in adulthood during routine cholesterol screening.

Treatment for Hyperlipoproteinemia Type II typically involves lifestyle modifications such as a heart-healthy diet, regular exercise, and weight loss. Medications such as statins, ezetimibe, and PCSK9 inhibitors may also be prescribed to lower LDL cholesterol levels and reduce the risk of cardiovascular disease.

Ultracentrifugation is a medical and laboratory technique used for the separation of particles of different sizes, densities, or shapes from a mixture based on their sedimentation rates. This process involves the use of a specialized piece of equipment called an ultracentrifuge, which can generate very high centrifugal forces, much greater than those produced by a regular centrifuge.

In ultracentrifugation, a sample is placed in a special tube and spun at extremely high speeds, causing the particles within the sample to separate based on their size, shape, and density. The larger or denser particles will sediment faster and accumulate at the bottom of the tube, while smaller or less dense particles will remain suspended in the solution or sediment more slowly.

Ultracentrifugation is a valuable tool in various fields, including biochemistry, molecular biology, and virology. It can be used to purify and concentrate viruses, subcellular organelles, membrane fractions, ribosomes, DNA, and other macromolecules from complex mixtures. The technique can also provide information about the size, shape, and density of these particles, making it a crucial method for characterizing and studying their properties.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Apolipoprotein C (apoC) is a group of proteins that are associated with lipoproteins, which are complex particles composed of lipids and proteins that play a crucial role in the transport and metabolism of lipids in the body. There are three main types of apoC proteins: apoC-I, apoC-II, and apoC-III.

ApoC-I is involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of cholesteryl ester transfer protein (CETP), which is an enzyme that facilitates the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL).

ApoC-II is a cofactor for lipoprotein lipase, an enzyme that hydrolyzes triglycerides in chylomicrons and VLDL, leading to the formation of smaller, denser lipoproteins. A deficiency in apoC-II can lead to hypertriglyceridemia, a condition characterized by elevated levels of triglycerides in the blood.

ApoC-III is also involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of lipoprotein lipase and CETP. Elevated levels of apoC-III have been associated with an increased risk of cardiovascular disease, possibly due to its effects on lipoprotein metabolism.

In summary, apolipoprotein C is a group of proteins that are involved in the regulation of lipoprotein metabolism and have important roles in the transport and metabolism of lipids in the body.

Lipase is an enzyme that is produced by the pancreas and found in the digestive system of most organisms. Its primary function is to catalyze the hydrolysis of fats (triglycerides) into smaller molecules, such as fatty acids and glycerol, which can then be absorbed by the intestines and utilized for energy or stored for later use.

In medical terms, lipase levels in the blood are often measured to diagnose or monitor conditions that affect the pancreas, such as pancreatitis (inflammation of the pancreas), pancreatic cancer, or cystic fibrosis. Elevated lipase levels may indicate damage to the pancreas and its ability to produce digestive enzymes.

Dietary cholesterol is a type of cholesterol that comes from the foods we eat. It is present in animal-derived products such as meat, poultry, dairy products, and eggs. While dietary cholesterol can contribute to an increase in blood cholesterol levels for some people, it's important to note that saturated and trans fats have a more significant impact on blood cholesterol levels than dietary cholesterol itself.

The American Heart Association recommends limiting dietary cholesterol intake to less than 300 milligrams per day for most people, and less than 200 milligrams per day for those with a history of heart disease or high cholesterol levels. However, individual responses to dietary cholesterol can vary, so it's essential to monitor blood cholesterol levels and adjust dietary habits accordingly.

Oxidation-Reduction (redox) reactions are a type of chemical reaction involving a transfer of electrons between two species. The substance that loses electrons in the reaction is oxidized, and the substance that gains electrons is reduced. Oxidation and reduction always occur together in a redox reaction, hence the term "oxidation-reduction."

In biological systems, redox reactions play a crucial role in many cellular processes, including energy production, metabolism, and signaling. The transfer of electrons in these reactions is often facilitated by specialized molecules called electron carriers, such as nicotinamide adenine dinucleotide (NAD+/NADH) and flavin adenine dinucleotide (FAD/FADH2).

The oxidation state of an element in a compound is a measure of the number of electrons that have been gained or lost relative to its neutral state. In redox reactions, the oxidation state of one or more elements changes as they gain or lose electrons. The substance that is oxidized has a higher oxidation state, while the substance that is reduced has a lower oxidation state.

Overall, oxidation-reduction reactions are fundamental to the functioning of living organisms and are involved in many important biological processes.

Hypertriglyceridemia is a medical condition characterized by an elevated level of triglycerides in the blood. Triglycerides are a type of fat (lipid) found in your blood that can increase the risk of developing heart disease, especially when levels are very high.

In general, hypertriglyceridemia is defined as having triglyceride levels greater than 150 milligrams per deciliter (mg/dL) of blood. However, the specific definition of hypertriglyceridemia may vary depending on individual risk factors and medical history.

Hypertriglyceridemia can be caused by a variety of factors, including genetics, obesity, physical inactivity, excessive alcohol consumption, and certain medications. In some cases, it may also be a secondary consequence of other medical conditions such as diabetes or hypothyroidism. Treatment for hypertriglyceridemia typically involves lifestyle modifications such as dietary changes, increased exercise, and weight loss, as well as medication if necessary.

Apolipoprotein B-48 (apoB-48) is a protein component of chylomicrons, which are lipoprotein particles responsible for carrying dietary fat and cholesterol from the intestines to other parts of the body. ApoB-48 is produced in the intestines and is a shorter version of apolipoprotein B-100 (apoB-100), which is a component of low-density lipoproteins (LDL) or "bad cholesterol."

Chylomicrons are assembled and secreted by intestinal cells after a meal, and apoB-48 is essential for the formation and function of these particles. ApoB-48-containing chylomicrons transport dietary lipids to various tissues, including the liver, where they contribute to the maintenance of lipid homeostasis.

Elevated levels of apoB-48 in the blood have been associated with an increased risk of cardiovascular disease, particularly in individuals with familial chylomicronemia syndrome (FCS), a rare genetic disorder characterized by severely elevated triglyceride levels due to impaired clearance of chylomicrons.

Lipid metabolism is the process by which the body breaks down and utilizes lipids (fats) for various functions, such as energy production, cell membrane formation, and hormone synthesis. This complex process involves several enzymes and pathways that regulate the digestion, absorption, transport, storage, and consumption of fats in the body.

The main types of lipids involved in metabolism include triglycerides, cholesterol, phospholipids, and fatty acids. The breakdown of these lipids begins in the digestive system, where enzymes called lipases break down dietary fats into smaller molecules called fatty acids and glycerol. These molecules are then absorbed into the bloodstream and transported to the liver, which is the main site of lipid metabolism.

In the liver, fatty acids may be further broken down for energy production or used to synthesize new lipids. Excess fatty acids may be stored as triglycerides in specialized cells called adipocytes (fat cells) for later use. Cholesterol is also metabolized in the liver, where it may be used to synthesize bile acids, steroid hormones, and other important molecules.

Disorders of lipid metabolism can lead to a range of health problems, including obesity, diabetes, cardiovascular disease, and non-alcoholic fatty liver disease (NAFLD). These conditions may be caused by genetic factors, lifestyle habits, or a combination of both. Proper diagnosis and management of lipid metabolism disorders typically involves a combination of dietary changes, exercise, and medication.

In the context of medical and health sciences, particle size generally refers to the diameter or dimension of particles, which can be in the form of solid particles, droplets, or aerosols. These particles may include airborne pollutants, pharmaceutical drugs, or medical devices such as nanoparticles used in drug delivery systems.

Particle size is an important factor to consider in various medical applications because it can affect the behavior and interactions of particles with biological systems. For example, smaller particle sizes can lead to greater absorption and distribution throughout the body, while larger particle sizes may be filtered out by the body's natural defense mechanisms. Therefore, understanding particle size and its implications is crucial for optimizing the safety and efficacy of medical treatments and interventions.

Hyperlipoproteinemias are medical conditions characterized by elevated levels of lipoproteins in the blood. Lipoproteins are particles that consist of proteins and lipids, which are responsible for transporting all fat molecules, such as cholesterol and triglycerides, around the body within the water outside cells. These lipids cannot dissolve in the blood, so they must be carried by these lipoprotein particles.

There are several types of hyperlipoproteinemias, classified based on the type of lipoprotein that is elevated and the pattern of inheritance. The most commonly recognized classification system is the Fredrickson classification, which includes five main types:

1. Type I - characterized by an excess of chylomicrons, a type of lipoprotein that carries dietary lipids, leading to extremely high levels of triglycerides in the blood. This rare disorder is usually caused by genetic mutations.
2. Type II - divided into two subtypes:
a. Type IIa - characterized by elevated LDL (low-density lipoprotein), or "bad" cholesterol, levels and often associated with premature cardiovascular disease. This condition can be caused by genetic factors, lifestyle choices, or both.
b. Type IIb - marked by increased levels of both LDL cholesterol and VLDL (very low-density lipoprotein), which leads to elevated triglycerides and cholesterol in the blood. This subtype can also be influenced by genetic factors, lifestyle choices, or both.
3. Type III - known as broad beta disease or remnant removal disease, this condition is characterized by an abnormal accumulation of remnant particles from VLDL and IDL (intermediate-density lipoprotein) metabolism, leading to increased levels of both cholesterol and triglycerides. This disorder can be caused by genetic mutations or secondary factors like diabetes, obesity, or hypothyroidism.
4. Type IV - characterized by elevated VLDL particles and high triglyceride levels in the blood. This condition is often associated with metabolic syndrome, obesity, diabetes, and alcohol consumption.
5. Type V - marked by increased VLDL and chylomicrons (lipoprotein particles that transport dietary lipids) in the blood, leading to extremely high triglyceride levels. This rare condition can be caused by genetic factors or secondary factors like diabetes, obesity, alcohol consumption, or uncontrolled lipid absorption.

It is important to note that these types are not mutually exclusive and can coexist in various combinations. Additionally, lifestyle choices such as diet, exercise, smoking, and alcohol consumption can significantly impact lipoprotein levels and contribute to the development of dyslipidemia (abnormal lipid levels).

Atherosclerosis is a medical condition characterized by the buildup of plaques, made up of fat, cholesterol, calcium, and other substances found in the blood, on the inner walls of the arteries. This process gradually narrows and hardens the arteries, reducing the flow of oxygen-rich blood to various parts of the body. Atherosclerosis can affect any artery in the body, including those that supply blood to the heart (coronary arteries), brain, limbs, and other organs. The progressive narrowing and hardening of the arteries can lead to serious complications such as coronary artery disease, carotid artery disease, peripheral artery disease, and aneurysms, which can result in heart attacks, strokes, or even death if left untreated.

The exact cause of atherosclerosis is not fully understood, but it is believed to be associated with several risk factors, including high blood pressure, high cholesterol levels, smoking, diabetes, obesity, physical inactivity, and a family history of the condition. Atherosclerosis can often progress without any symptoms for many years, but as the disease advances, it can lead to various signs and symptoms depending on which arteries are affected. Treatment typically involves lifestyle changes, medications, and, in some cases, surgical procedures to restore blood flow.

Cholesteryl ester transfer proteins (CETP) are a group of plasma proteins that play a role in the transport and metabolism of lipids, particularly cholesteryl esters and triglycerides, between different lipoprotein particles in the bloodstream. These proteins facilitate the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), while simultaneously promoting the transfer of triglycerides in the opposite direction, from VLDL and LDL to HDL.

The net effect of CETP activity is a decrease in HDL cholesterol levels and an increase in LDL and VLDL cholesterol levels. This shift in lipoprotein composition can contribute to the development of atherosclerosis and cardiovascular disease, as lower HDL cholesterol levels and higher LDL cholesterol levels are associated with increased risk for these conditions.

Inhibition of CETP has been investigated as a potential strategy for increasing HDL cholesterol levels and reducing the risk of cardiovascular disease. However, clinical trials with CETP inhibitors have shown mixed results, and further research is needed to determine their safety and efficacy in preventing cardiovascular events.

Scavenger receptors are a class of cell surface receptors that play a crucial role in the recognition and clearance of various biomolecules, including modified self-molecules, pathogens, and apoptotic cells. These receptors are expressed mainly by phagocytic cells such as macrophages and dendritic cells, but they can also be found on other cell types, including endothelial cells and smooth muscle cells.

Scavenger receptors have broad specificity and can bind to a wide range of ligands, including oxidized low-density lipoprotein (oxLDL), polyanionic molecules, advanced glycation end products (AGEs), and pathogen-associated molecular patterns (PAMPs). The binding of ligands to scavenger receptors triggers various cellular responses, such as phagocytosis, endocytosis, signaling cascades, and the production of cytokines and chemokines.

Scavenger receptors are classified into several families based on their structural features and ligand specificity, including:

1. Class A (SR-A): This family includes SR-AI, SR-AII, and MARCO, which bind to oxLDL, bacteria, and apoptotic cells.
2. Class B (SR-B): This family includes SR-BI, CD36, and LIMPII, which bind to lipoproteins, phospholipids, and pathogens.
3. Class C (SR-C): This family includes DEC-205, MRC1, and LOX-1, which bind to various ligands, including apoptotic cells, bacteria, and oxLDL.
4. Class D (SR-D): This family includes SCARF1, which binds to PAMPs and damage-associated molecular patterns (DAMPs).
5. Class E (SR-E): This family includes CXCL16, which binds to chemokine CXCR6 and phosphatidylserine.

Scavenger receptors play a critical role in maintaining tissue homeostasis by removing damaged or altered molecules and cells, modulating immune responses, and regulating lipid metabolism. Dysregulation of scavenger receptor function has been implicated in various pathological conditions, including atherosclerosis, inflammation, infection, and cancer.

Apolipoprotein A-II (ApoA-II) is a protein component of high-density lipoproteins (HDL), often referred to as "good cholesterol." It is one of the major apolipoproteins in HDL and plays a role in the structure, metabolism, and function of HDL particles. ApoA-II is produced primarily in the liver and intestine and helps facilitate the transport of cholesterol from tissues to the liver for excretion. Additionally, ApoA-II has been shown to have anti-inflammatory properties and may play a role in the regulation of the immune response.

Apolipoprotein C-III (APOC3) is a protein that is produced in the liver and circulates in the bloodstream. It is a component of certain lipoproteins, including very low-density lipoproteins (VLDL) and chylomicrons, which are responsible for transporting fat molecules, such as triglycerides and cholesterol, throughout the body.

APOC3 plays a role in regulating the metabolism of these lipoproteins. Specifically, it inhibits the activity of an enzyme called lipoprotein lipase, which breaks down triglycerides in VLDL and chylomicrons. As a result, high levels of APOC3 can lead to an increase in triglyceride levels in the blood, which is a risk factor for cardiovascular disease.

Genetic variations in the APOC3 gene have been associated with differences in triglyceride levels and risk of cardiovascular disease. Some studies have suggested that reducing APOC3 levels through genetic editing or other means may be a promising strategy for lowering triglycerides and reducing the risk of heart disease.

Dietary fats, also known as fatty acids, are a major nutrient that the body needs for energy and various functions. They are an essential component of cell membranes and hormones, and they help the body absorb certain vitamins. There are several types of dietary fats:

1. Saturated fats: These are typically solid at room temperature and are found in animal products such as meat, butter, and cheese, as well as tropical oils like coconut and palm oil. Consuming a high amount of saturated fats can raise levels of unhealthy LDL cholesterol and increase the risk of heart disease.
2. Unsaturated fats: These are typically liquid at room temperature and can be further divided into monounsaturated and polyunsaturated fats. Monounsaturated fats, found in foods such as olive oil, avocados, and nuts, can help lower levels of unhealthy LDL cholesterol while maintaining levels of healthy HDL cholesterol. Polyunsaturated fats, found in foods such as fatty fish, flaxseeds, and walnuts, have similar effects on cholesterol levels and also provide essential omega-3 and omega-6 fatty acids that the body cannot produce on its own.
3. Trans fats: These are unsaturated fats that have been chemically modified to be solid at room temperature. They are often found in processed foods such as baked goods, fried foods, and snack foods. Consuming trans fats can raise levels of unhealthy LDL cholesterol and lower levels of healthy HDL cholesterol, increasing the risk of heart disease.

It is recommended to limit intake of saturated and trans fats and to consume more unsaturated fats as part of a healthy diet.

Phospholipids are a major class of lipids that consist of a hydrophilic (water-attracting) head and two hydrophobic (water-repelling) tails. The head is composed of a phosphate group, which is often bound to an organic molecule such as choline, ethanolamine, serine or inositol. The tails are made up of two fatty acid chains.

Phospholipids are a key component of cell membranes and play a crucial role in maintaining the structural integrity and function of the cell. They form a lipid bilayer, with the hydrophilic heads facing outwards and the hydrophobic tails facing inwards, creating a barrier that separates the interior of the cell from the outside environment.

Phospholipids are also involved in various cellular processes such as signal transduction, intracellular trafficking, and protein function regulation. Additionally, they serve as emulsifiers in the digestive system, helping to break down fats in the diet.

Scavenger receptors, class B (SR-B) are a type of scavenger receptors that play a crucial role in the cellular uptake and metabolism of lipids, particularly modified low-density lipoproteins (LDL), high-density lipoproteins (HDL), and other lipid-soluble molecules. They are membrane-bound glycoproteins that contain an extracellular domain with a characteristic structure, including cysteine-rich repeats and transmembrane domains.

The best-characterized member of this class is SR-B1 (also known as CD36b, SCARB1), which is widely expressed in various tissues, such as the liver, steroidogenic organs, macrophages, and endothelial cells. SR-B1 selectively binds to HDL and facilitates the transfer of cholesteryl esters from HDL particles into cells while allowing HDL to maintain its structural integrity and continue its function in reverse cholesterol transport.

SR-B1 has also been implicated in the uptake and degradation of oxidized LDL, contributing to the development of atherosclerosis. Additionally, SR-B1 is involved in several other cellular processes, including innate immunity, inflammation, and angiogenesis.

Other members of class B scavenger receptors include SR-BI, SR-B2 (also known as CLA-1 or LIMPII), SR-B3 (also known as CD36c or SCARB2), and SR-B4 (also known as CXorf24). These receptors have distinct expression patterns and functions but share structural similarities with SR-BI.

In summary, scavenger receptors, class B, are a group of membrane-bound glycoproteins that facilitate the cellular uptake and metabolism of lipids, particularly modified LDL and HDL particles. They play essential roles in maintaining lipid homeostasis and have implications in various pathological conditions, such as atherosclerosis and inflammation.

Anticholesteremic agents are a class of medications that are used to lower the levels of cholesterol and other fats called lipids in the blood. These medications work by reducing the production of cholesterol in the body, increasing the removal of cholesterol from the bloodstream, or preventing the absorption of cholesterol in the digestive tract.

There are several types of anticholesteremic agents, including:

1. Statins: These medications work by blocking a liver enzyme that is necessary for the production of cholesterol. Examples of statins include atorvastatin, simvastatin, and rosuvastatin.
2. Bile acid sequestrants: These medications bind to bile acids in the digestive tract and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which in turn lowers cholesterol levels. Examples of bile acid sequestrants include cholestyramine and colesevelam.
3. Nicotinic acid: Also known as niacin, this medication works by reducing the production of very low-density lipoproteins (VLDL) in the liver, which are a major source of bad cholesterol.
4. Fibrates: These medications work by increasing the removal of cholesterol from the bloodstream and reducing the production of VLDL in the liver. Examples of fibrates include gemfibrozil and fenofibrate.
5. PCSK9 inhibitors: These are a newer class of medications that work by blocking the action of a protein called PCSK9, which helps regulate the amount of cholesterol in the blood. By blocking PCSK9, these medications increase the number of LDL receptors on the surface of liver cells, which leads to increased removal of LDL from the bloodstream.

Anticholesteremic agents are often prescribed for people who have high cholesterol levels and are at risk for heart disease or stroke. By lowering cholesterol levels, these medications can help reduce the risk of heart attack, stroke, and other cardiovascular events.

Phosphatidylcholine-Sterol O-Acyltransferase (PCOAT, also known as Sterol O-Acyltransferase 1 or SOAT1) is an enzyme that plays a crucial role in the regulation of cholesterol metabolism. It is located in the endoplasmic reticulum and is responsible for the transfer of acyl groups from phosphatidylcholine to cholesterol, forming cholesteryl esters. This enzymatic reaction results in the storage of excess cholesterol in lipid droplets, preventing its accumulation in the cell membrane and potentially contributing to the development of atherosclerosis if not properly regulated.

Defects or mutations in PCOAT can lead to disruptions in cholesterol homeostasis, which may contribute to various diseases such as cardiovascular disorders, metabolic syndrome, and neurodegenerative conditions. Therefore, understanding the function and regulation of this enzyme is essential for developing therapeutic strategies aimed at managing cholesterol-related disorders.

Apolipoprotein C-II (ApoC-II) is a type of apolipoprotein, which are proteins that bind to lipids to form lipoprotein complexes. ApoC-II is a component of several lipoproteins, including very low-density lipoproteins (VLDL) and chylomicrons, which are responsible for the transport of fat molecules, such as triglycerides and cholesterol, in the bloodstream.

ApoC-II plays a crucial role in the activation of lipoprotein lipase, an enzyme that breaks down triglycerides in VLDL and chylomicrons into fatty acids, which can then be taken up by cells for energy production or storage. Therefore, ApoC-II deficiency can lead to hypertriglyceridemia, a condition characterized by high levels of triglycerides in the blood.

In addition to its role in lipid metabolism, ApoC-II has been implicated in the development and progression of atherosclerosis, a chronic inflammatory disease that affects the arteries and can lead to serious cardiovascular complications, such as heart attack and stroke.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Foam cells are a type of cell that form when certain white blood cells, called macrophages, accumulate an excessive amount of lipids (fats) within their cytoplasm. This occurs due to the ingestion and breakdown of low-density lipoproteins (LDL), which then get trapped inside the macrophages, leading to the formation of large lipid-rich vacuoles that give the cells a foamy appearance under the microscope.

Foam cells are commonly found in the early stages of atherosclerosis, a condition characterized by the buildup of plaque in the walls of arteries. Over time, the accumulation of foam cells and other components of plaque can narrow or block the affected artery, leading to serious health problems such as heart attack or stroke.

Macrophages are a type of white blood cell that are an essential part of the immune system. They are large, specialized cells that engulf and destroy foreign substances, such as bacteria, viruses, parasites, and fungi, as well as damaged or dead cells. Macrophages are found throughout the body, including in the bloodstream, lymph nodes, spleen, liver, lungs, and connective tissues. They play a critical role in inflammation, immune response, and tissue repair and remodeling.

Macrophages originate from monocytes, which are a type of white blood cell produced in the bone marrow. When monocytes enter the tissues, they differentiate into macrophages, which have a larger size and more specialized functions than monocytes. Macrophages can change their shape and move through tissues to reach sites of infection or injury. They also produce cytokines, chemokines, and other signaling molecules that help coordinate the immune response and recruit other immune cells to the site of infection or injury.

Macrophages have a variety of surface receptors that allow them to recognize and respond to different types of foreign substances and signals from other cells. They can engulf and digest foreign particles, bacteria, and viruses through a process called phagocytosis. Macrophages also play a role in presenting antigens to T cells, which are another type of immune cell that helps coordinate the immune response.

Overall, macrophages are crucial for maintaining tissue homeostasis, defending against infection, and promoting wound healing and tissue repair. Dysregulation of macrophage function has been implicated in a variety of diseases, including cancer, autoimmune disorders, and chronic inflammatory conditions.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

CD36 is a type of protein found on the surface of certain cells in the human body, including platelets, white blood cells (monocytes and macrophages), and fat (adipose) cells. It is a type of scavenger receptor that plays a role in various biological processes, such as:

1. Fatty acid uptake and metabolism: CD36 helps facilitate the transport of long-chain fatty acids into cells for energy production and storage.
2. Inflammation and immune response: CD36 is involved in the recognition and clearance of foreign substances (pathogens) and damaged or dying cells, which can trigger an immune response.
3. Angiogenesis: CD36 has been implicated in the regulation of blood vessel formation (angiogenesis), particularly during wound healing and tumor growth.
4. Atherosclerosis: CD36 has been associated with the development and progression of atherosclerosis, a condition characterized by the buildup of fats, cholesterol, and other substances in and on the artery walls. This is due to its role in the uptake of oxidized low-density lipoprotein (oxLDL) by macrophages, leading to the formation of foam cells and the development of fatty streaks in the arterial wall.
5. Infectious diseases: CD36 has been identified as a receptor for various pathogens, including malaria parasites, HIV, and some bacteria, which can use this protein to gain entry into host cells.

As an antigen, CD36 is a molecule that can be targeted by the immune system to produce an immune response. Antibodies against CD36 have been found in various diseases, such as autoimmune disorders and certain infections. Modulation of CD36 activity has been suggested as a potential therapeutic strategy for several conditions, including atherosclerosis, diabetes, and infectious diseases.

Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).

Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.

Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.

Esterification is a chemical reaction that involves the conversion of an alcohol and a carboxylic acid into an ester, typically through the removal of a molecule of water. This reaction is often catalyzed by an acid or a base, and it is a key process in organic chemistry. Esters are commonly found in nature and are responsible for the fragrances of many fruits and flowers. They are also important in the production of various industrial and consumer products, including plastics, resins, and perfumes.

Hyperlipoproteinemia Type I, also known as Familial Lipoprotein Lipase Deficiency, is a rare genetic disorder characterized by an absence or deficiency of the enzyme lipoprotein lipase. This enzyme is responsible for breaking down chylomicrons, which are large lipoprotein particles that transport dietary triglycerides from the intestines to the liver and peripheral tissues.

As a result of this deficiency, chylomicrons accumulate in the bloodstream, leading to elevated levels of triglycerides (hypertriglyceridemia) and chylomicrons (chylomiconemia). This condition can cause eruptive xanthomas, which are collections of lipid-laden foam cells that form under the skin, and recurrent pancreatitis, which is inflammation of the pancreas.

Hyperlipoproteinemia Type I is inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene, one from each parent, to develop the condition. Treatment typically involves a low-fat diet and medications to reduce triglyceride levels.

Heparin is defined as a highly sulfated glycosaminoglycan (a type of polysaccharide) that is widely present in many tissues, but is most commonly derived from the mucosal tissues of mammalian lungs or intestinal mucosa. It is an anticoagulant that acts as an inhibitor of several enzymes involved in the blood coagulation cascade, primarily by activating antithrombin III which then neutralizes thrombin and other clotting factors.

Heparin is used medically to prevent and treat thromboembolic disorders such as deep vein thrombosis, pulmonary embolism, and certain types of heart attacks. It can also be used during hemodialysis, cardiac bypass surgery, and other medical procedures to prevent the formation of blood clots.

It's important to note that while heparin is a powerful anticoagulant, it does not have any fibrinolytic activity, meaning it cannot dissolve existing blood clots. Instead, it prevents new clots from forming and stops existing clots from growing larger.

Dyslipidemia is a condition characterized by an abnormal amount of cholesterol and/or triglycerides in the blood. It can be caused by genetic factors, lifestyle habits such as poor diet and lack of exercise, or other medical conditions such as diabetes or hypothyroidism.

There are several types of dyslipidemias, including:

1. Hypercholesterolemia: This is an excess of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. High levels of LDL cholesterol can lead to the formation of plaque in the arteries, increasing the risk of heart disease and stroke.
2. Hypertriglyceridemia: This is an excess of triglycerides, a type of fat found in the blood, which can also contribute to the development of plaque in the arteries.
3. Mixed dyslipidemia: This is a combination of high LDL cholesterol and high triglycerides.
4. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol, also known as "good" cholesterol, helps remove LDL cholesterol from the blood. Low levels of HDL cholesterol can increase the risk of heart disease and stroke.

Dyslipidemias often do not cause any symptoms but can be detected through a blood test that measures cholesterol and triglyceride levels. Treatment typically involves lifestyle changes such as eating a healthy diet, getting regular exercise, and quitting smoking. In some cases, medication may also be necessary to lower cholesterol or triglyceride levels.

Lipid peroxidation is a process in which free radicals, such as reactive oxygen species (ROS), steal electrons from lipids containing carbon-carbon double bonds, particularly polyunsaturated fatty acids (PUFAs). This results in the formation of lipid hydroperoxides, which can decompose to form a variety of compounds including reactive carbonyl compounds, aldehydes, and ketones.

Malondialdehyde (MDA) is one such compound that is commonly used as a marker for lipid peroxidation. Lipid peroxidation can cause damage to cell membranes, leading to changes in their fluidity and permeability, and can also result in the modification of proteins and DNA, contributing to cellular dysfunction and ultimately cell death. It is associated with various pathological conditions such as atherosclerosis, neurodegenerative diseases, and cancer.

Familial Combined Hyperlipidemia (FCH) is a genetic disorder characterized by high levels of cholesterol and/or fats (lipids) in the blood. It is one of the most common inherited lipid disorders, affecting approximately 1 in 200 to 1 in 500 people.

FCH is caused by mutations in several genes involved in lipid metabolism, including the APOB, LDLR, and PCSK9 genes. These genetic defects lead to increased levels of low-density lipoprotein (LDL) cholesterol, triglycerides, or both in the blood.

Individuals with FCH may have elevated levels of total cholesterol, LDL cholesterol, and/or triglycerides, which can increase their risk for premature atherosclerosis and cardiovascular disease. The condition often presents in early adulthood and may manifest as mixed hyperlipidemia (high levels of both LDL cholesterol and triglycerides) or isolated hypercholesterolemia (high levels of LDL cholesterol only).

Familial combined hyperlipidemia is typically managed with lifestyle modifications, such as a heart-healthy diet, regular exercise, and weight management. Medications, such as statins, may also be prescribed to lower lipid levels and reduce the risk of cardiovascular disease. Regular monitoring of lipid levels is essential for effective management and prevention of complications associated with FCH.

Lipolysis is the process by which fat cells (adipocytes) break down stored triglycerides into glycerol and free fatty acids. This process occurs when the body needs to use stored fat as a source of energy, such as during fasting, exercise, or in response to certain hormonal signals. The breakdown products of lipolysis can be used directly by cells for energy production or can be released into the bloodstream and transported to other tissues for use. Lipolysis is regulated by several hormones, including adrenaline (epinephrine), noradrenaline (norepinephrine), cortisol, glucagon, and growth hormone, which act on lipases, enzymes that mediate the breakdown of triglycerides.

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as statins, are a class of cholesterol-lowering medications. They work by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. By blocking this enzyme, the liver is stimulated to take up more low-density lipoprotein (LDL) cholesterol from the bloodstream, leading to a decrease in LDL cholesterol levels and a reduced risk of cardiovascular disease.

Examples of HMG-CoA reductase inhibitors include atorvastatin, simvastatin, pravastatin, rosuvastatin, and fluvastatin. These medications are commonly prescribed to individuals with high cholesterol levels, particularly those who are at risk for or have established cardiovascular disease.

It's important to note that while HMG-CoA reductase inhibitors can be effective in reducing LDL cholesterol levels and the risk of cardiovascular events, they should be used as part of a comprehensive approach to managing high cholesterol, which may also include lifestyle modifications such as dietary changes, exercise, and weight management.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

Fatty acids are carboxylic acids with a long aliphatic chain, which are important components of lipids and are widely distributed in living organisms. They can be classified based on the length of their carbon chain, saturation level (presence or absence of double bonds), and other structural features.

The two main types of fatty acids are:

1. Saturated fatty acids: These have no double bonds in their carbon chain and are typically solid at room temperature. Examples include palmitic acid (C16:0) and stearic acid (C18:0).
2. Unsaturated fatty acids: These contain one or more double bonds in their carbon chain and can be further classified into monounsaturated (one double bond) and polyunsaturated (two or more double bonds) fatty acids. Examples of unsaturated fatty acids include oleic acid (C18:1, monounsaturated), linoleic acid (C18:2, polyunsaturated), and alpha-linolenic acid (C18:3, polyunsaturated).

Fatty acids play crucial roles in various biological processes, such as energy storage, membrane structure, and cell signaling. Some essential fatty acids cannot be synthesized by the human body and must be obtained through dietary sources.

The aorta is the largest artery in the human body, which originates from the left ventricle of the heart and carries oxygenated blood to the rest of the body. It can be divided into several parts, including the ascending aorta, aortic arch, and descending aorta. The ascending aorta gives rise to the coronary arteries that supply blood to the heart muscle. The aortic arch gives rise to the brachiocephalic, left common carotid, and left subclavian arteries, which supply blood to the head, neck, and upper extremities. The descending aorta travels through the thorax and abdomen, giving rise to various intercostal, visceral, and renal arteries that supply blood to the chest wall, organs, and kidneys.

Medical Definition of Vitamin E:

Vitamin E is a fat-soluble antioxidant that plays a crucial role in protecting your body's cells from damage caused by free radicals, which are unstable molecules produced when your body breaks down food or is exposed to environmental toxins like cigarette smoke and radiation. Vitamin E is also involved in immune function, DNA repair, and other metabolic processes.

It is a collective name for a group of eight fat-soluble compounds that include four tocopherols and four tocotrienols. Alpha-tocopherol is the most biologically active form of vitamin E in humans and is the one most commonly found in supplements.

Vitamin E deficiency is rare but can occur in people with certain genetic disorders or who cannot absorb fat properly. Symptoms of deficiency include nerve and muscle damage, loss of feeling in the arms and legs, muscle weakness, and vision problems.

Food sources of vitamin E include vegetable oils (such as sunflower, safflower, and wheat germ oil), nuts and seeds (like almonds, peanuts, and sunflower seeds), and fortified foods (such as cereals and some fruit juices).

Hyperlipoproteinemia Type IV is a genetic disorder characterized by an increased level of very low-density lipoproteins (VLDL) in the blood. This leads to elevated levels of triglycerides, which are a type of fat found in the blood. The condition is also sometimes referred to as "Fredrickson Type IV."

People with Hyperlipoproteinemia Type IV have an increased risk of developing pancreatitis, a potentially life-threatening inflammation of the pancreas, due to high levels of triglycerides. They may also have an increased risk of cardiovascular disease due to elevated levels of VLDL and other atherogenic lipoproteins.

The condition is usually inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disorder if one parent has it. However, some cases may be caused by mutations in multiple genes or by environmental factors such as obesity, diabetes, and excessive alcohol consumption.

Treatment for Hyperlipoproteinemia Type IV typically involves lifestyle modifications such as weight loss, exercise, and dietary changes to reduce triglyceride levels. In some cases, medication may be necessary to control the condition.

Hypolipoproteinemias are a group of genetic disorders characterized by low levels of lipoproteins in the blood. Lipoproteins are complex particles composed of proteins and lipids that play a crucial role in the transport and metabolism of fat molecules, such as cholesterol and triglycerides, in the body.

There are several types of hypolipoproteinemias, each associated with deficiencies in specific lipoproteins:

1. Hypobetalipoproteinemia: This disorder is characterized by low levels of beta-lipoproteins, also known as low-density lipoproteins (LDL), or "bad" cholesterol. It can lead to decreased absorption of fat-soluble vitamins and an increased risk of fatty liver disease.
2. Abetalipoproteinemia: This is a rare autosomal recessive disorder characterized by the absence of beta-lipoproteins and apolipoprotein B, which results in very low levels of LDL cholesterol and high-density lipoproteins (HDL), or "good" cholesterol. It can lead to fat malabsorption, neurological symptoms, and retinal degeneration.
3. Tangier disease: This disorder is caused by a deficiency in apolipoprotein A-I and results in low levels of HDL cholesterol. It can cause enlarged orange-colored tonsils, neuropathy, and an increased risk of coronary artery disease.
4. Familial hypoalphalipoproteinemia: This disorder is characterized by low levels of HDL cholesterol due to a deficiency in apolipoprotein A-I or A-II. It can increase the risk of premature coronary artery disease.

It's important to note that while some hypolipoproteinemias are associated with an increased risk of cardiovascular disease, others may actually protect against it due to reduced levels of atherogenic lipoproteins. Treatment for these disorders typically involves dietary modifications and supplementation of fat-soluble vitamins and essential fatty acids. In some cases, medication may be necessary to manage symptoms or prevent complications.

Triolein is a type of triglyceride, which is a kind of fat molecule. More specifically, triolein is the triglyceride formed from three molecules of oleic acid, a common monounsaturated fatty acid. It is often used in scientific research and studies involving lipid metabolism, and it can be found in various vegetable oils and animal fats.

Electrophoresis, polyacrylamide gel (EPG) is a laboratory technique used to separate and analyze complex mixtures of proteins or nucleic acids (DNA or RNA) based on their size and electrical charge. This technique utilizes a matrix made of cross-linked polyacrylamide, a type of gel, which provides a stable and uniform environment for the separation of molecules.

In this process:

1. The polyacrylamide gel is prepared by mixing acrylamide monomers with a cross-linking agent (bis-acrylamide) and a catalyst (ammonium persulfate) in the presence of a buffer solution.
2. The gel is then poured into a mold and allowed to polymerize, forming a solid matrix with uniform pore sizes that depend on the concentration of acrylamide used. Higher concentrations result in smaller pores, providing better resolution for separating smaller molecules.
3. Once the gel has set, it is placed in an electrophoresis apparatus containing a buffer solution. Samples containing the mixture of proteins or nucleic acids are loaded into wells on the top of the gel.
4. An electric field is applied across the gel, causing the negatively charged molecules to migrate towards the positive electrode (anode) while positively charged molecules move toward the negative electrode (cathode). The rate of migration depends on the size, charge, and shape of the molecules.
5. Smaller molecules move faster through the gel matrix and will migrate farther from the origin compared to larger molecules, resulting in separation based on size. Proteins and nucleic acids can be selectively stained after electrophoresis to visualize the separated bands.

EPG is widely used in various research fields, including molecular biology, genetics, proteomics, and forensic science, for applications such as protein characterization, DNA fragment analysis, cloning, mutation detection, and quality control of nucleic acid or protein samples.

Aryldialkylphosphatases are a group of enzymes that catalyze the hydrolysis of certain types of organophosphate compounds. Specifically, they break down compounds that contain an aryl (aromatic) group linked to two alkyl groups through a phosphorus atom. These enzymes play a role in the detoxification of these compounds in living organisms.

The medical definition of 'Aryldialkylphosphatase' is not commonly used, as it refers to a specific type of enzyme that is not typically discussed in a clinical context. However, understanding the function of these enzymes can be important for toxicologists and other researchers who study the effects of organophosphate compounds on living systems.

Medical Definition:

"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.

Lovastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. It works by inhibiting HMG-CoA reductase, an enzyme that plays a crucial role in the production of cholesterol in the body. By reducing the amount of cholesterol produced in the liver, lovastatin helps to decrease the levels of low-density lipoprotein (LDL) or "bad" cholesterol and triglycerides in the blood, while increasing the levels of high-density lipoprotein (HDL) or "good" cholesterol.

Lovastatin is available in both immediate-release and extended-release forms, and it is typically taken orally once or twice a day, depending on the dosage prescribed by a healthcare provider. Common side effects of lovastatin include headache, nausea, diarrhea, and muscle pain, although more serious side effects such as liver damage and muscle weakness are possible, particularly at higher doses.

It is important to note that lovastatin should not be taken by individuals with active liver disease or by those who are pregnant or breastfeeding. Additionally, it may interact with certain other medications, so it is essential to inform a healthcare provider of all medications being taken before starting lovastatin therapy.

Abetalipoproteinemia is a rare inherited genetic disorder that affects the way the body absorbs and metabolizes fats and fat-soluble vitamins. It is caused by mutations in the genes responsible for producing proteins involved in the formation and transport of beta-lipoproteins, which are necessary for the absorption of dietary fats and cholesterol from the intestines.

Individuals with abetalipoproteinemia are unable to produce adequate levels of these lipoproteins, leading to a deficiency in fat-soluble vitamins (A, D, E, and K) and an accumulation of fats in the intestines. This results in various symptoms such as steatorrhea (fatty, foul-smelling stools), malabsorption, diarrhea, failure to thrive, and neurological issues due to vitamin E deficiency.

The disorder is typically diagnosed in infancy or early childhood and requires lifelong dietary management, including a low-fat diet and supplementation with fat-soluble vitamins. Early intervention can help prevent the progression of neurological symptoms and improve overall prognosis.

Probucol is not a medication that has a widely accepted or commonly used medical definition in the same way that many other medications do. However, probucol is a type of drug that was developed for use in treating cardiovascular disease. It is a cholesterol-lowering agent and antioxidant that was previously used in the management of hypercholesterolemia (high levels of cholesterol in the blood).

Probucol works by reducing the amount of low-density lipoprotein (LDL) or "bad" cholesterol in the body, which can help to lower the risk of heart disease and stroke. It is also believed to have antioxidant properties, which may help to protect against the damaging effects of free radicals on the body's cells.

Despite its potential benefits, probucol is not commonly used in clinical practice today due to concerns about its safety and efficacy. Some studies have suggested that probucol may be associated with an increased risk of death from heart disease, as well as other serious side effects. As a result, it is generally not recommended for use in the treatment of hypercholesterolemia or any other medical conditions.

Scavenger receptors, class E (SR-E), also known as CD36 and scavenger receptor family member 8 (SCARF8), are a group of membrane-bound receptors found on the surface of various cell types, including macrophages, platelets, and endothelial cells. They play a crucial role in the recognition and clearance of damaged or modified self-molecules, as well as foreign substances, from the body.

SR-E receptors have a wide range of ligands, such as oxidized low-density lipoprotein (oxLDL), apoptotic cells, bacteria, and long-chain fatty acids. The binding of these ligands to SR-E triggers various intracellular signaling pathways that regulate cellular processes like phagocytosis, foam cell formation, inflammation, and lipid metabolism.

Dysregulation of SR-E receptors has been implicated in several diseases, including atherosclerosis, diabetes, obesity, and Alzheimer's disease. Therefore, understanding the function and regulation of these receptors can provide valuable insights into the pathogenesis of various disorders and potentially lead to the development of novel therapeutic strategies.

Sterol O-Acyltransferase (SOAT, also known as ACAT for Acyl-CoA:cholesterol acyltransferase) is an enzyme that plays a crucial role in cholesterol homeostasis within cells. Specifically, it catalyzes the reaction of esterifying free cholesterol with fatty acyl-coenzyme A (fatty acyl-CoA) to form cholesteryl esters. This enzymatic activity allows for the intracellular storage of excess cholesterol in lipid droplets, reducing the levels of free cholesterol in the cell and thus preventing its potential toxic effects on membranes and proteins. There are two isoforms of SOAT, SOAT1 and SOAT2, which exhibit distinct subcellular localization and functions. Dysregulation of SOAT activity has been implicated in various pathological conditions, including atherosclerosis and neurodegenerative disorders.

Apolipoprotein E3 (ApoE3) is one of the three major isoforms of apolipoprotein E (ApoE), a protein involved in the metabolism of lipids, particularly cholesterol. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4. These alleles result in three main isoforms of the protein: ApoE2, ApoE3, and ApoE4.

ApoE3 is the most common isoform, found in approximately 77-78% of the population. It has a slightly different amino acid sequence compared to ApoE2 and ApoE4, which can affect its function. ApoE3 is thought to play a neutral or protective role in the risk of developing Alzheimer's disease and cardiovascular diseases, although some studies suggest that it may have a mildly favorable effect on lipid metabolism compared to ApoE4.

Electrophoresis, Agar Gel is a laboratory technique used to separate and analyze DNA, RNA, or proteins based on their size and electrical charge. In this method, the sample is mixed with agarose gel, a gelatinous substance derived from seaweed, and then solidified in a horizontal slab-like format. An electric field is applied to the gel, causing the negatively charged DNA or RNA molecules to migrate towards the positive electrode. The smaller molecules move faster through the gel than the larger ones, resulting in their separation based on size. This technique is widely used in molecular biology and genetics research, as well as in diagnostic testing for various genetic disorders.

Biological transport refers to the movement of molecules, ions, or solutes across biological membranes or through cells in living organisms. This process is essential for maintaining homeostasis, regulating cellular functions, and enabling communication between cells. There are two main types of biological transport: passive transport and active transport.

Passive transport does not require the input of energy and includes:

1. Diffusion: The random movement of molecules from an area of high concentration to an area of low concentration until equilibrium is reached.
2. Osmosis: The diffusion of solvent molecules (usually water) across a semi-permeable membrane from an area of lower solute concentration to an area of higher solute concentration.
3. Facilitated diffusion: The assisted passage of polar or charged substances through protein channels or carriers in the cell membrane, which increases the rate of diffusion without consuming energy.

Active transport requires the input of energy (in the form of ATP) and includes:

1. Primary active transport: The direct use of ATP to move molecules against their concentration gradient, often driven by specific transport proteins called pumps.
2. Secondary active transport: The coupling of the movement of one substance down its electrochemical gradient with the uphill transport of another substance, mediated by a shared transport protein. This process is also known as co-transport or counter-transport.

Coronary artery disease, often simply referred to as coronary disease, is a condition in which the blood vessels that supply oxygen-rich blood to the heart become narrowed or blocked due to the buildup of fatty deposits called plaques. This can lead to chest pain (angina), shortness of breath, or in severe cases, a heart attack.

The medical definition of coronary artery disease is:

A condition characterized by the accumulation of atheromatous plaques in the walls of the coronary arteries, leading to decreased blood flow and oxygen supply to the myocardium (heart muscle). This can result in symptoms such as angina pectoris, shortness of breath, or arrhythmias, and may ultimately lead to myocardial infarction (heart attack) or heart failure.

Risk factors for coronary artery disease include age, smoking, high blood pressure, high cholesterol, diabetes, obesity, physical inactivity, and a family history of the condition. Lifestyle changes such as quitting smoking, exercising regularly, eating a healthy diet, and managing stress can help reduce the risk of developing coronary artery disease. Medical treatments may include medications to control blood pressure, cholesterol levels, or irregular heart rhythms, as well as procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Immunologic receptors are specialized proteins found on the surface of immune cells that recognize and bind to specific molecules, known as antigens, on the surface of pathogens or infected cells. This binding triggers a series of intracellular signaling events that activate the immune cell and initiate an immune response.

There are several types of immunologic receptors, including:

1. T-cell receptors (TCRs): These receptors are found on the surface of T cells and recognize antigens presented in the context of major histocompatibility complex (MHC) molecules.
2. B-cell receptors (BCRs): These receptors are found on the surface of B cells and recognize free antigens in solution.
3. Pattern recognition receptors (PRRs): These receptors are found inside immune cells and recognize conserved molecular patterns associated with pathogens, such as lipopolysaccharides and flagellin.
4. Fc receptors: These receptors are found on the surface of various immune cells and bind to the constant region of antibodies, mediating effector functions such as phagocytosis and antibody-dependent cellular cytotoxicity (ADCC).

Immunologic receptors play a critical role in the recognition and elimination of pathogens and infected cells, and dysregulation of these receptors can lead to immune disorders and diseases.

An atherogenic diet is a type of eating pattern that can contribute to the development and progression of atherosclerosis, which is the hardening and narrowing of the arteries due to the buildup of fats, cholesterol, and other substances in the inner lining of the artery walls.

An atherogenic diet is typically high in saturated and trans fats, cholesterol, refined carbohydrates, and salt, and low in fiber, fruits, vegetables, and unsaturated fats. This type of diet can increase the levels of LDL (low-density lipoprotein) or "bad" cholesterol in the blood, which can lead to the formation of plaques in the arteries and increase the risk of cardiovascular disease, including heart attack and stroke.

Therefore, it is recommended to follow a heart-healthy diet that emphasizes fruits, vegetables, whole grains, lean proteins, and healthy fats to reduce the risk of atherosclerosis and other chronic diseases.

Apolipoprotein C-I (apoC-I) is a small protein component of lipoproteins, which are particles that transport all fat molecules (lipids), including cholesterol, in the bloodstream. ApoC-I is primarily produced in the liver and intestines and plays a crucial role in the metabolism of triglyceride-rich lipoproteins, such as very low-density lipoproteins (VLDL) and chylomicrons.

Apolipoprotein C-I has several functions:

1. Inhibition of lipoprotein lipase (LPL): ApoC-I inhibits the activity of LPL, an enzyme responsible for breaking down triglycerides in lipoproteins. This inhibition helps regulate the rate at which fatty acids are released from triglyceride-rich lipoproteins and taken up by cells for energy production or storage.
2. Activation of hepatic lipase (HL): ApoC-I activates HL, an enzyme involved in the catabolism of intermediate-density lipoproteins (IDL) and high-density lipoproteins (HDL). This activation aids in the clearance of these particles from the circulation.
3. Regulation of cholesterol efflux: ApoC-I may also play a role in regulating cholesterol efflux, the process by which excess cholesterol is removed from cells and transported to the liver for excretion.

Genetic variations in the APOC1 gene, which encodes apoC-I, have been associated with alterations in lipid metabolism and an increased risk of cardiovascular disease.

Hyperlipoproteinemia Type III, also known as Broad Beta Disease or Remnant Hyperlipidemia, is a genetic disorder characterized by an increased level of chylomicron remnants and intermediate-density lipoproteins (IDL) in the blood. This results in elevated levels of both low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, and decreased levels of high-density lipoprotein (HDL), or "good" cholesterol. The condition can lead to premature atherosclerosis and an increased risk for cardiovascular disease. It is caused by mutations in the APOE gene, which encodes the apolipoprotein E protein, leading to abnormal clearance of lipoproteins from the blood.

Lipid peroxides are chemical compounds that form when lipids (fats or fat-like substances) oxidize. This process, known as lipid peroxidation, involves the reaction of lipids with oxygen in a way that leads to the formation of hydroperoxides and various aldehydes, such as malondialdehyde.

Lipid peroxidation is a naturally occurring process that can also be accelerated by factors such as exposure to radiation, certain chemicals, or enzymatic reactions. It plays a role in many biological processes, including cell signaling and regulation of gene expression, but it can also contribute to the development of various diseases when it becomes excessive.

Examples of lipid peroxides include phospholipid hydroperoxides, cholesteryl ester hydroperoxides, and triglyceride hydroperoxides. These compounds are often used as markers of oxidative stress in biological systems and have been implicated in the pathogenesis of atherosclerosis, cancer, neurodegenerative diseases, and other conditions associated with oxidative damage.

LDL-Receptor Related Proteins (LRP) are a family of single transmembrane domain receptors that play important roles in various cellular processes, including endocytosis, intracellular signaling, and protein degradation. They are named after their structural and functional similarities to the low-density lipoprotein (LDL) receptor.

The LDL-Receptor Related Proteins consist of several members, including LRP1, LRP2 (also known as Megalin), LRP3, LRP4, LRP5, and LRP6. These proteins are widely expressed in various tissues, such as the brain, liver, kidney, and muscle.

LRP1 is a large receptor that is involved in the clearance of several ligands, including LDL, apolipoprotein E (apoE), and α2-macroglobulin. It also plays a role in intracellular signaling pathways related to cell survival, differentiation, and migration.

LRP2 is primarily expressed in the kidney and the brain, where it functions as a scavenger receptor that mediates the endocytosis of various ligands, including lipoproteins, vitamin-binding proteins, and enzymes.

LRP3 is involved in the clearance of apoE-containing lipoproteins and has been implicated in the regulation of cholesterol metabolism.

LRP4 is a critical regulator of neuromuscular junction formation and function, and it interacts with several ligands, including agrin and LDL.

LRP5 and LRP6 are involved in the Wnt signaling pathway, which plays important roles in embryonic development, tissue homeostasis, and cancer. They act as co-receptors for Wnt proteins and modulate intracellular signaling pathways that regulate gene expression and cell behavior.

Overall, LDL-Receptor Related Proteins play diverse and critical roles in various physiological processes, and their dysfunction has been implicated in several diseases, including neurodegenerative disorders, cardiovascular disease, and cancer.

Oleic acid is a monounsaturated fatty acid that is commonly found in various natural oils such as olive oil, sunflower oil, and grapeseed oil. Its chemical formula is cis-9-octadecenoic acid, and it is a colorless liquid at room temperature. Oleic acid is an important component of human diet and has been shown to have potential health benefits, including reducing the risk of heart disease and improving immune function. It is also used in the manufacture of soaps, cosmetics, and other personal care products.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Apoproteins are the protein components of lipoprotein complexes, which are responsible for transporting fat molecules, such as cholesterol and triglycerides, throughout the body. Apoproteins play a crucial role in the metabolism of lipids by acting as recognition signals that allow lipoproteins to interact with specific receptors on cell surfaces.

There are several different types of apoproteins, each with distinct functions. For example, apolipoprotein A-1 (apoA-1) is the major protein component of high-density lipoproteins (HDL), which are responsible for transporting excess cholesterol from tissues to the liver for excretion. Apolipoprotein B (apoB) is a large apoprotein found in low-density lipoproteins (LDL), very low-density lipoproteins (VLDL), and lipoprotein(a). ApoB plays a critical role in the assembly and secretion of VLDL from the liver, and it also mediates the uptake of LDL by cells.

Abnormalities in apoprotein levels or function can contribute to the development of various diseases, including cardiovascular disease, diabetes, and Alzheimer's disease. Therefore, measuring apoprotein levels in the blood can provide valuable information for diagnosing and monitoring these conditions.

Oleic acid is a monounsaturated fatty acid that is commonly found in various natural oils such as olive oil, sunflower oil, and peanut oil. Its chemical formula is cis-9-octadecenoic acid, and it is a colorless liquid at room temperature with a slight odor. Oleic acid is an important component of human diet and has been shown to have various health benefits, including reducing the risk of heart disease and improving immune function. It is also used in the manufacture of soaps, cosmetics, and other industrial products.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Lysophosphatidylcholines (LPCs) are a type of glycerophospholipids, which are major components of cell membranes. They are formed by the hydrolysis of phosphatidylcholines, another type of glycerophospholipids, catalyzed by the enzyme phospholipase A2. LPCs contain a single fatty acid chain attached to a glycerol backbone and a choline headgroup.

In medical terms, LPCs have been implicated in various physiological and pathological processes, such as cell signaling, membrane remodeling, and inflammation. Elevated levels of LPCs have been found in several diseases, including cardiovascular disease, neurodegenerative disorders, and cancer. They can also serve as biomarkers for the diagnosis and prognosis of these conditions.

Fasting is defined in medical terms as the abstinence from food or drink for a period of time. This practice is often recommended before certain medical tests or procedures, as it helps to ensure that the results are not affected by recent eating or drinking.

In some cases, fasting may also be used as a therapeutic intervention, such as in the management of seizures or other neurological conditions. Fasting can help to lower blood sugar and insulin levels, which can have a variety of health benefits. However, it is important to note that prolonged fasting can also have negative effects on the body, including malnutrition, dehydration, and electrolyte imbalances.

Fasting is also a spiritual practice in many religions, including Christianity, Islam, Buddhism, and Hinduism. In these contexts, fasting is often seen as a way to purify the mind and body, to focus on spiritual practices, or to express devotion or mourning.

... low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL delivers fat molecules to cells. LDL is involved in ... There are two other assays for LDL particles, however, like LDL-C, most only estimate LDL particle concentrations. Direct LDL ... releasing LDL. LDL is then shipped to the lysosome, where cholesterol esters in the LDL are hydrolysed. LDL receptors are ... Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein that transport all fat molecules around the body ...
In humans, the LDL receptor protein is encoded by the LDLR gene on chromosome 19. It belongs to the low density lipoprotein ... 7 LDL-R class A domains, and 6 LDL-R class B repeats. The N-terminal domain of the LDL receptor, which is responsible for ... LDL receptor mediates the endocytosis of cholesterol-rich LDL and thus maintains the plasma level of LDL. This occurs in all ... The low-density lipoprotein receptor (LDL-R) is a mosaic protein of 839 amino acids (after removal of 21-amino acid signal ...
Because of the high cost of directly measuring HDL and LDL (low-density lipoprotein) protein particles, blood tests are ... High-density lipoprotein (HDL) is one of the five major groups of lipoproteins. Lipoproteins are complex particles composed of ... This is often contrasted with the amount of cholesterol estimated to be carried within low-density lipoprotein particles, LDL, ... As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The ...
... lb LDL). large buoyant LDL (lb LDL) particles small dense LDL (sd LDL) particles Lipoprotein(a) (LPA) is a lipoprotein particle ... LDL particles are sometimes referred to as "bad" lipoprotein because concentrations of two kinds of LDL (sd-LDL and LPA), ... Binding of LDL to its target tissue occurs through an interaction between the LDL receptor and apolipoprotein B-100 on the LDL ... LDL, IDL, VLDL and chylomicrons. The handling of lipoprotein particles in the body is referred to as lipoprotein particle ...
Schematic representation of the seven mammalian LDL receptor (LDLR) family members LDL receptor family members LDL+Receptors at ... LDL) and removed by the liver via endocytosis of the LDL receptor. Recent evidence indicates that the members of the LDL ... The low-density lipoprotein receptor gene family codes for a class of structurally related cell surface receptors that fulfill ... These modules are: LDL receptor type A (LA) repeats of 40 residues each, displaying a triple-disulfide-bond-stabilized ...
Pentikäinen MO, Oksjoki R, Oörni K, Kovanen PT (2002). "Lipoprotein lipase in the arterial wall: linking LDL to the arterial ... NIH/UW entry on Familial Lipoprotein Lipase Deficiency Gene therapy for lipoprotein lipase deficiency Lipoprotein+lipase at the ... "Entrez Gene: LPL lipoprotein lipase". Wang H, Eckel RH (2009). "Lipoprotein lipase: from gene to obesity". Am J Physiol ... Lipoprotein lipase (LPL) (EC 3.1.1.34, systematic name triacylglycerol acylhydrolase (lipoprotein-dependent)) is a member of ...
Low density lipoproteins are made up of cholesterol, TG, phospholipids, and apolipoproteins. LDL-C molecules bind to the ... These agents reduce LDL-C, increase HDL-C, decrease triglycerides, and decrease lipoprotein(a). The FOURNIER and ODYSSEY trials ... and low density lipoprotein cholesterol (LDL-C). High triglyceride levels (>1.7 mmol/L fasting) can indicate dyslipidemia. ... This causes high amounts of LDL and VLDL molecules to form. A unique sign of primary dyslipidemias is that patients will often ...
Lipids analyzed are LDL (low-density lipoproteins), triglyceride, and apolipoprotein B levels. A patient could be diagnosed ... In patients with only CMRD, lipid panels are expected to display normal triglyceride levels, but LDL and HDL levels may >50% ...
In the blood Lp-PLA2 travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density ... "The role of lipoprotein-associated phospholipase A2 in atherosclerosis may depend on its lipoprotein carrier in plasma". ... Lipoprotein-associated phospholipase A2 (Lp-PLA2) also known as platelet-activating factor acetylhydrolase (PAF-AH) is a ... May 2010). "Lipoprotein-associated phospholipase A(2) and risk of coronary disease, stroke, and mortality: collaborative ...
Transferrin and beta-lipoprotein (LDL) comprises the beta-1. Increased beta-1 protein due to the increased level of free ... Even staining in this zone is due to alpha-1 lipoprotein (high density lipoprotein - HDL). Decrease occurs in severe ... There are low levels in inflammation and high levels in pregnancy.[citation needed] Beta lipoprotein forms an irregular ... Increased beta-1 protein due to LDL elevation occurs in hypercholesterolemia. Decreased beta-1 protein occurs in acute or ...
... consumption raises low-density lipoprotein (LDL) cholesterol. Merck Index, 11th Edition, 6246 Bond, Andrew D. ( ... "Effects of saturated fatty acids on serum lipids and lipoproteins: a systematic review and regression analysis" (PDF). World ...
Deposits have been found to consist mostly of low-density lipoprotein (LDL). Deposition of lipids into the cornea begins at the ... AS is caused by leakage of lipoproteins from limbal capillaries into the corneal stroma. ...
LDL is a low-density lipoprotein, one of the five major groups of lipoproteins. LDL or LdL may also refer to: Learning by ... Look up LDL in Wiktionary, the free dictionary. ... page lists articles associated with the title LDL. If an ... whereby students learn by themselves teaching Loudness discomfort level in hyperacusis LDL decomposition, Cholesky ...
On the contrary, Low-density lipoprotein (LDL) cholesterol works in opposition. LDL cholesterol does not transport cholesterol ... LIPG regulates lipoprotein metabolism through the hydrolysis of HDL phospholipids. This high-density lipoprotein is an ... LDL should be kept low in the body to avoid cholesterol buildup in arteries. When HDL are hydrolyzed, the turnover rate of HDL ... These processes include lipoprotein metabolism, cytokine expression, and lipid composition in cells. Unlike the lipases that ...
... which are the precursor to low-density lipoproteins (LDL). These reductions increase the number of cellular LDL receptors, thus ... Overall, the result is a reduction in circulating cholesterol and LDL. A minor reduction in triglycerides and an increase in ... Pravastatin has been shown to have a similar effectiveness at lowering low-density lipoprotein cholesterol as other statin ... Pravastatin acts as a lipoprotein-lowering drug through two pathways. In the major pathway, pravastatin inhibits the function ...
"Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL". Journal of Lipid Research. 39 (4): 777- ... oxidized low density lipoprotein, native lipoproteins, oxidized phospholipids, and long-chain fatty acids. Work in genetically ... Nicholson AC, Frieda S, Pearce A, Silverstein RL (February 1995). "Oxidized LDL binds to CD36 on human monocyte-derived ... Zeng Y, Tao N, Chung KN, Heuser JE, Lublin DM (November 2003). "Endocytosis of oxidized low density lipoprotein through ...
"Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL". Journal of Lipid Research. 39 (4): 777- ... Graham DL, Oram JF (June 1987). "Identification and characterization of a high density lipoprotein-binding protein in cell ...
LDL apheresis - removal of low density lipoprotein in patients with familial hypercholesterolemia. Lipoprotein(a) (Lp(a) ... "Lipoprotein (a)". CDC Office of Science (OS), Office of Genomics and Precision Public Health. U.S. Department of Health & Human ...
... plaques with modified low density lipoprotein (LDL) are formed. GITR expression was detected in plaques macrophages and T cells ...
"The 39-kDa receptor-associated protein modulates lipoprotein catabolism by binding to LDL receptors". The Journal of Biological ... LRP gives protection across LDL by LRPAP and its downregulation may be subjected for an elevation of LDL and Ab-related ... "The very low density lipoprotein receptor mediates the cellular catabolism of lipoprotein lipase and urokinase-plasminogen ... Low density lipoprotein receptor-related protein-associated protein 1 also known as LRPAP1 or RAP is a chaperone protein which ...
This is coupled with significantly increased low-density lipoprotein (LDL) receptor expression. Diagnosis is made by measuring ...
Serum low-density lipoprotein-cholesterol (LDL-C) was also decreased by DOM. Further, the total cholesterol levels of subjects ... "Drinking Deep Seawater Decreases Serum Total and Low-Density Lipoprotein-Cholesterol in Hypercholesterolemic Subjects". Journal ...
Lipoprotein apheresis therapy is another nonsurgical treatment for reducing LDL-C concentrations. PCSK9 inhibitors are a new ... and a type of lipoprotein is called high density lipoprotein (HDL). A high concentration of high density lipoproteins- ... Another factor of CVD that is often overlooked involves the concentrations of low-density lipoproteins (LDL) and very low- ... Statins are a class of drugs used to treat cardiovascular disease by lowering lipid levels, specifically LDL-C levels. Statins ...
They are present in various lipoprotein complexes, including HDL, LDL and VLDL. GRCh38: Ensembl release 89: ENSG00000184831 - ...
VLDL is converted in the bloodstream to low-density lipoprotein (LDL) and intermediate-density lipoprotein (IDL). VLDL ... they become LDL, with apoB-100 as the primary apolipoprotein. The LDL is taken into a cell via the LDL receptor via endocytosis ... intermediate-density lipoprotein, low-density lipoprotein, high-density lipoprotein) that enable fats and cholesterol to move ... Very-low-density lipoprotein (VLDL), density relative to extracellular water, is a type of lipoprotein made by the liver. VLDL ...
Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase. The LDL receptor scavenges circulating LDL ... low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Lower protein/lipid ratios make for less dense lipoproteins ... Since higher blood LDL - especially higher LDL concentrations and smaller LDL particle size - contributes to this process more ... Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL, rather than the total cholesterol level, correlate with the ...
It can be associated with LDL receptor. Associated regions and genes include: niacin is sometimes prescribed to raise HDL ... Hypoalphalipoproteinemia is a high-density lipoprotein deficiency, inherited in an autosomal dominant manner. ... September 2005). "Combined monogenic hypercholesterolemia and hypoalphalipoproteinemia caused by mutations in LDL-R and LCAT ...
The effects of rosuvastatin on low-density lipoprotein (LDL) cholesterol are dose-related. Higher doses were more efficacious ... Meta-analysis showed that rosuvastatin is able to modestly increase levels of high-density lipoprotein (HDL) cholesterol as ... Rosuvastatin is approved in the United States for the treatment of high LDL cholesterol (dyslipidemia), total cholesterol ( ... McTaggart F (August 2008). "Effects of statins on high-density lipoproteins: a potential contribution to cardiovascular benefit ...
MK-4 is carried by the same lipoproteins (TRL, LDL, and HDL) and cleared fast as well. The long-chain menaquinones are absorbed ... Most of vitamin K1 is carried by triacylglycerol-rich lipoproteins (TRL) and rapidly cleared by the liver; only a small amount ... Schurgers LJ, Vermeer C (February 2002). "Differential lipoprotein transport pathways of K-vitamins in healthy subjects". ... in the same way as vitamin K1 and MK-4, but are efficiently redistributed by the liver in predominantly LDL (VLDL). Since LDL ...
The envelope of HCV is similar to very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL). Because of this ... It could surround itself with lipoproteins, partially covering up E1 and E2. Recent research indicates that these ... LDL receptor, SR-BI, DC-SIGN, Claudin-1, and Occludin. ... SR-B1 is able to remove lipids from the lipoproteins around the ...
Finally, secreted LDL and HDL lipoprotein particles are also enclosed by a lipid monolayer. The formation of these structures ...
... a genetic disorder characterized by high low-density lipoprotein [LDL] cholesterol levels) was significantly lower than among ... also plays an important role in regulating low-density lipoprotein (LDL) cholesterol levels. ... Controlling low-density lipoprotein-cholesterol levels: an interview with Jay Edelberg, M.D., Sanofi and Bill Sasiela, Ph.D., ... Estrogen plays key role in regulating blood pressure, LDL cholesterol levels What makes some women more susceptible to heart ...
E-LDL is recognised by the C1q subunit of C1 and triggers direct C1 activation, suggesting that complement activation by E-LDL ... Recently we have studied the ability of an enzymatically modified form of LDL (E-LDL), obtained by treatment with trypsin and ... When incorporated into vesicles, the lipid fraction of E-LDL, but not of native LDL, triggered C1 activation, and activation ... low density lipoproteins) in the extracellular matrix of the blood vessels. These LDL particles are modified by a number of ...
The ERS-education website provides centralised access to all educational material produced by the European Respiratory Society. It is the worlds largest CME collection for lung diseases and treatment offering high quality e-learning and teaching resources for respiratory specialists. This distance learning portal contains up-to-date study material for the state-of-the-art in Pulmonology.
LDL direct blood testing can give some people a more accurate measurement of their bad cholesterol than a standard Lipid Panel ... The Low Density Lipoprotein Cholesterol (direct) test is used to evaluate a persons risk for heart disease. LDL is often ... The Low Density Lipoprotein Cholesterol (direct) test is used to evaluate a persons risk for heart disease. LDL is often ... The Low Density Lipoprotein Cholesterol (direct) test is used to evaluate a persons risk for heart disease. LDL is often ...
Markedly increased levels of mildly modified LDL subfractions, such as dense LDL and electronegatively charged LDL (LDL,sup,-,/ ... LDL,sup,-,/sup,, characterized by modified protein content and elevated levels of lipid peroxidation products, is ... In this review, we discussed known mechanisms leading to that may account for oxidative protein modification and/or LDL,sup,-,/ ... representative of multiple oxidative processes acting on plasma lipoproteins that prevail during HD. ...
ANALISIS KANDUNGAN LOGAM BERAT TIMBAL (Pb) Low Density Lipoprotein (LDL) dan High Density Lipoprotein (HDL) PADA KERANG DARAH ( ... Heavy Metal Weight; Lead (Pb) , Low density lipoprotein (LDL) High density lipoproteins (HDL) ; Blood Clams (Anadara granosa ... IRMA DINIARTI, 141411131037 (2019) ANALISIS KANDUNGAN LOGAM BERAT TIMBAL (Pb) Low Density Lipoprotein (LDL) dan High Density ... Parameter utama yang diamati dalam penelitian ini adalah konsentrasi logam berat timbal (Pb), LDL dan HDL. Dari hasil ...
... low-density lipoproteins cholesterol (LDL-C), and triglycerides. The present file provides data on LDL-C and triglycerides. ... Calculated LDL-C LEVELS. Serum LDL-C levels were derived on study participants examined in the morning session only. LDL-C is ... Cholesterol - Low-Density Lipoproteins (LDL) & Triglycerides (P_TRIGLY). Data File: P_TRIGLY.xpt. First Published: October 2021 ... LBDLDLN - LDL-Cholesterol, NIH equation 2 (mg/dL). Variable Name: LBDLDLN. SAS Label: LDL-Cholesterol, NIH equation 2 (mg/dL). ...
Low-density lipoprotein (LDL) cholesterol. People sometimes refer to this as "bad" cholesterol. High LDL levels cause plaque to ... high levels of LDL cholesterol usually do not cause symptoms. As a result, individuals are often unaware of the high levels ... High-density lipoprotein (HDL) cholesterol. People sometimes call this "good" cholesterol. Therefore, low HDL levels may also ... Overweight and obesity raise LDL cholesterol and lower HDL cholesterol. Losing as little as 5-10%. of body weight can improve ...
2 Raising High-Density Lipoprotein (HDL) 3 Lowering Low-Density Lipoprotein (LDL) ... Ask your doctor if you should take medication to lower LDL. Due to age, disability, or other health issues, your body may not ... Eat certain foods to lower LDL. Consume oats, whole grains and high-fiber foods. Brazil nuts, almonds and walnuts may help ... Red wine especially has been linked to higher HDL and even lower LDL levels.[12] X Trustworthy Source MedlinePlus Collection of ...
Differences between Lp(a) and LDL. / Gorges, Roland; Hofer, G.; Sommer, Andreas et al. in: Journal of Lipid Research, Jahrgang ... Differences between Lp(a) and LDL",. author = "Roland Gorges and G. Hofer and Andreas Sommer and Herbert St{u}tz and H. ... Differences between Lp(a) and LDL. Roland Gorges, G. Hofer, Andreas Sommer, Herbert Stütz, H. Grillhofer, G.M. Kostner , ... Differences between Lp(a) and LDL. in: Journal of Lipid Research. 1995 ; Jahrgang 36. S. 251-259. ...
LDL, HDL, chylomicron, VLDL and their components cholesterol, cholesterol ester, triglycerides, apoprotein. - Alila Medical ... Lipoproteins of the blood, LDL, HDL, chylomicron, VLDL. Molecular structure of lipoproteins of the blood: LDL, HDL, chylomicron ... Molecular structure of lipoproteins of the blood: ...
10 Foods That Lower Low-Density Lipoprotein (LDL) "Bad" Cholesterol. March 1, 2022by Mamta Kothiwale ... Learn about the effects of LDL "bad" cholesterol and foods that can lower LDL and help reduce the risks. ...
There was no difference in serum cholesterol/high-density lipoprotein (HDL)-C and low-density lipoprotein (LDL)-C/HDL-C ratios ...
In humans, the LDL receptor protein is encoded by the LDLR gene on chromosome 19. It belongs to the low density lipoprotein ... 7 LDL-R class A domains, and 6 LDL-R class B repeats. The N-terminal domain of the LDL receptor, which is responsible for ... LDL receptor mediates the endocytosis of cholesterol-rich LDL and thus maintains the plasma level of LDL. This occurs in all ... The low-density lipoprotein receptor (LDL-R) is a mosaic protein of 839 amino acids (after removal of 21-amino acid signal ...
Whereas most studies have demonstrated a strong association between lipoprotein (a) and the presence and severi … ... The role of lipoprotein (a) in the atherosclerotic process is continually being unraveled, and many of its potential ... As a consequence of its interaction with LDL, alternative strategies for treating high levels of lipoprotein (a) will be ... is modulated by concomitant LDL-cholesterol levels. Such a modulation of the pathogenicity of lipoprotein (a) may underlie the ...
Alan T. Remaley, seeks to better understand lipoprotein metabolism and to translate new insights gained from b ... have shared their equation calculator for low-density lipoprotein cholesterol (LDL-C), called Sampson-NIH equation for LDL-C. ... Lipoprotein Metabolism. The Lipoprotein Metabolism Laboratory, led by Dr. Alan T. Remaley, seeks to better understand ... dynamic regulation by circulating lipoproteins and enzymes. Dr. Remaleys laboratory seeks to better understand lipoprotein ...
... a study found that Collinsella correlates with higher serum levels of total cholesterol and low-density lipoprotein (LDL) ...
... high-density lipoprotein; HIV = human immunodeficiency virus.; IUD = intrauterine device; LDL = low-density lipoprotein; LNG- ...
The two most commonly known lipoproteins are low-density lipoproteins (LDL) and high-density lipoproteins (HDL). ... What is LDL (low-density lipoprotein) cholesterol? This type of cholesterol is commonly called "bad" cholesterol. It can ... LDL levels should be low. To help lower LDL levels, children and adolescents should:. *Avoid foods high in saturated and trans ... What is HDL (high-density lipoprotein) cholesterol? This type of cholesterol is known as "good" cholesterol, and is a type of ...
... high-density lipoprotein; HIV = human immunodeficiency virus; LDL = low-density lipoprotein; LNG-IUD = levonorgestrel-releasing ... high LDL, or high triglyceride levels). 1. 2. 2. 3. 2. 3/4. Implants, DMPA, POP: When multiple major risk factors exist, risk ...
... and low-density lipoprotein cholesterol (LDL-C) levels. We investigated whether nurse-led, telephone-based follow-up was more ... LDL-C , 2.5 mmol/L). Results At 12 months, mean systolic BP, diastolic BP and LDL-C was 3.3 (95% CI 0.3 to 6.3) mmHg, 2.3 mmHg ... Among participants with values above the treatment goal at baseline, the difference in systolic BP and LDL-C was more ... 56.8%, p = 0.008) and LDL-C (69.7% vs. 50.4%, p , 0.001). Conclusions Nurse-led, telephone-based secondary preventive follow-up ...
... or high-density lipoprotein, is the good cholesterol. It helps to remove bad cholesterol from your arteries, so a higher HDL ... What are HDL and LDL?. HDL and LDL are two types of lipoproteins.They are a combination of fat (lipid) and protein. The lipids ... LDL stands for low-density lipoproteins. It is sometimes called the "bad" cholesterol because a high LDL level leads to a ... HDL and LDL have different purposes:. *HDL stands for high-density lipoproteins. It is sometimes called the "good" cholesterol ...
LDL) receptors: the prototypic LDL receptor (LDLR) along with the LDL receptor-related protein 1 (LRP1). Although each are ... Ng lipoproteins are taken up by two functionally significant low-density lipoprotein ( ... Ng lipoproteins are taken up by two functionally significant low-density lipoprotein (LDL) receptors: the prototypic LDL ... Ng lipoproteins are taken up by two functionally significant low-density lipoprotein (LDL) receptors: the prototypic ...
FOCAL REGIONS OF INCREASED ARTERIAL PERMEABILITY TO LOW-DENSITY-LIPOPROTEIN (LDL) INVIVO MEASURED BY AUTORADIOGRAPHY. Title. ... FOCAL REGIONS OF INCREASED ARTERIAL PERMEABILITY TO LOW-DENSITY-LIPOPROTEIN (LDL) INVIVO MEASURED BY AUTORADIOGRAPHY. ...
... study Highlights From the study Very low LDL cholesterol is associated with increased all-cause mortality.Very low LDL ... The association of repeatedly measured low-density lipoprotein cholesterol and all-cause mortality and cardiovascular disease ... The association of repeatedly measured low-density lipoprotein cholesterol and all-cause mortality and cardiovascular disease ... Very low LDL cholesterol is associated with increased all-cause mortality.. *Very low LDL cholesterol is not associated with ...
An elevated total cholesterol or low density lipoprotein (LDL) cholesterol level and/or a reduced high density lipoprotein (HDL ... high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, TG = triglycerides. ... high-density lipoprotein cholesterol, LDL-C = low-density lipoprotein cholesterol, TG = triglycerides. ... In patients with clinical atherosclerotic cardiovascular disease (ASCVD), reduce low-density lipoprotein cholesterol (LDL-C) ...
N/D: no data; ABCGs: ATP-binding cassette, subfamily G transporters; LDL-R: low-density lipoprotein receptor. L-ORACFL: ... The oil reduced levels of total cholesterol, triglycerides and direct low-density lipoprotein cholesterol (LDL-c) but increased ... ox-LDL: Low Density Lipoproteins. NLRP3: nod-like receptor pyrin containing 3; p38-MAPK: p38 mitogen-activated protein kinase; ... showed reduced levels of ROS and oxidized-low density lipoproteins (ox-LDL) along with an increased activity of antioxidative ...
Abbreviations used: ANA, antinuclear antibody; HDL, high density lipoprotein; LDL, low density lipoprotein; OD, odds ratio. ... Review of efficacy and safety of use of higher doses of statins to achieve lower LDL cholesterol levels; ALT elevations are ... simvastatin lowers total serum cholesterol and particularly low density lipoprotein (LDL) cholesterol concentrations, thereby ... Systematic review of relationship between LDL cholesterol lowering effects and adverse events in 23 statin treatment arms ...
j The serum TC and LDL-C. k The liver TC and FC. TC, total cholesterol; LDL-C, low-density lipoprotein cholesterol; FC, free ... f Serum TC and g serum LDL-C levels and h liver TC and i liver FC content. TC, total cholesterol; LDL-C, low-density ... TC, total cholesterol; LDL-C, low-density lipoprotein cholesterol; FC, free cholesterol. Data are represented by the mean ± SEM ... We also investigated the effect of FSH in LDL receptor deficiency (ldlr-/-) mice. The results showed that the serum TC and LDL- ...
  • Arterial inflammation that precedes development of the atherosclerotic plaque is caused by accumulation of LDL (low density lipoproteins) in the extracellular matrix of the blood vessels. (europa.eu)
  • 2018). The blood lipids measurements in NHANES include total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoproteins cholesterol (LDL-C), and triglycerides. (cdc.gov)
  • The two most commonly known lipoproteins are low-density lipoproteins (LDL) and high-density lipoproteins (HDL). (choc.org)
  • HDL stands for high-density lipoproteins. (medlineplus.gov)
  • LDL stands for low-density lipoproteins. (medlineplus.gov)
  • CNT also dose-dependently induced low density lipoproteins (LDL) oxidation in the presence of HAECs. (cdc.gov)
  • With a standard Lipid Panel Cholesterol Test, the LDL measurement is calculated using a person's Total Cholesterol, HDL, and Triglycerides. (requestatest.com)
  • The present file provides data on LDL-C and triglycerides. (cdc.gov)
  • This method to measure triglycerides is based on the work by Wahlefeld (Roche, 2014) using a lipoprotein lipase from microorganisms for the rapid and complete hydrolysis of triglycerides to glycerol followed by oxidation to dihydroxyacetone phosphate and hydrogen peroxide. (cdc.gov)
  • Serum LDL-C levels were calculated from directly measured values of total cholesterol, triglycerides, and HDL-C. Please see below the Data Processing and Editing section for more details. (cdc.gov)
  • LDL particles are formed when triglycerides are removed from VLDL by the lipoprotein lipase enzyme (LPL) and they become smaller and denser (i.e. fewer fat molecules with same protein transport shell), containing a higher proportion of cholesterol esters. (wikipedia.org)
  • Learn more about cholesterol, LDL, HDL and triglycerides in children and adolescents. (choc.org)
  • A full lipid profile shows the actual levels of each type of fat in the blood, such as LDL, HDL, triglycerides and total cholesterol. (choc.org)
  • Hyperlipidemia comprises a heterogeneous group of disorders, characterized by high levels in one or more lipids and/or lipoproteins [atherogenic free fatty acids (FA), triglycerides (TG) (hypertriglyceridemia), small dense low-density lipoprotein cholesterol (LDL-C) (hypercholesterolemia), and apolipoprotein (apo) B], and/or low level in antiatherogenic high density lipoprotein cholesterol (HDL-C), in the circulation [ 1 - 3 ]. (hindawi.com)
  • [ 1 , 2 ] However, there is growing evidence that triglycerides are not just a marker of increased cardiovascular (CV) risk but rather a causal factor that rivals LDL-C. [ 3 ] Madsen et al . (medscape.com)
  • Defining the cholesterol content in these triglyceride-rich lipoproteins is clinically important because this is the substrate for development of the atherosclerotic plaque rather than the triglycerides. (medscape.com)
  • Therefore, there is delayed conversion of VLDL to LDL, resulting in elevation in TRL-C. Since lipolysis is impaired, LDL particles are also enriched in apoCIII and triglycerides which ultimately transform into smaller and more numerous particles. (medscape.com)
  • [ 13 ] If triglycerides are lowered by lifestyle changes, fibrates, or omega-3 fatty acids, there is a reduction in TRL-C, apoB, and apoCIII, and this shifts from small dense LDL particles (and hence small dense LDL-C) to larger LDL particles. (medscape.com)
  • Lipoproteins transfer lipids (fats) around the body in the extracellular fluid, making fats available to body cells for receptor-mediated endocytosis. (wikipedia.org)
  • Effects of plant stanol esters supplied in low-fat yoghurt on serum lipids and lipoproteins, non-cholesterol sterols and fat soluble antioxidant concentrations. (tci-thaijo.org)
  • These groups, from least dense to most dense, are chylomicrons (aka ULDL by the overall density naming convention), very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). (wikipedia.org)
  • 12] Screening should commence at 2 years trial, small very low-density lipoprotein (VLDL), small high- of age if there is a family history of hypercholesterolaemia, early density lipoprotein (HDL), medium low-density lipoprotein (LDL) cardiovascular disease or if the family history is unknown. (who.int)
  • [ 6 ] The confusion arises as to what to call this "other" cholesterol (non-HDL-C minus LDL-C). The most accurate term is triglyceride-rich lipoprotein cholesterol (TRL-C) but it has also been called 'remnant cholesterol' [ 7 ] and most commonly VLDL-C. (medscape.com)
  • characterized by modified protein content and elevated levels of lipid peroxidation products, is representative of multiple oxidative processes acting on plasma lipoproteins that prevail during HD. (scienceopen.com)
  • Transfer of phospholipase A-resistant pyrene-dialkyl-glycerophosphocholine to plasma lipoproteins. (elsevierpure.com)
  • A major class of molecules involved in heart disease are the plasma lipoproteins. (otago.ac.nz)
  • High cardiovascular mortality in patients on hemodialysis (HD) is largely attributed to oxidative stress and altered lipoprotein profiles. (scienceopen.com)
  • The common clinical interpretation of blood lipid levels is that high LDL is associated with increased risk of cardiovascular diseases. (wikipedia.org)
  • The Lipoprotein Metabolism Laboratory, led by Dr. Alan T. Remaley, seeks to better understand lipoprotein metabolism and to translate new insights gained from basic biochemistry, cell biology, and transgenic animal models into much-needed clinical advances in the treatment and prevention of cardiovascular disease. (nih.gov)
  • Very low LDL cholesterol is associated with increased all-cause mortality but not statistically associated with cardiovascular disease incidence among dyslipidemic patients, regardless of risk. (drstevesikorsky.com)
  • Both of these types of fat increase your LDL cholesterol , making you prone to cardiovascular disorders. (medicinenet.com)
  • Reduction of total cholesterols (TC) and LDL-C by dietary alterations and medications that affect lipid metabolism [ 14 ] is found to reduce the occurrence of atherosclerosis in animals and clinical cardiovascular events in human [ 15 ]. (hindawi.com)
  • LDL is often referred to as the "bad" cholesterol because it carries cholesterol into the arteries. (requestatest.com)
  • LDL is involved in atherosclerosis, a process in which it is oxidized within the walls of arteries. (wikipedia.org)
  • It is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries. (medlineplus.gov)
  • LDL can clog your arteries. (medlineplus.gov)
  • LDL, also called "bad" cholesterol, can cause buildup of plaque on the walls of arteries. (scdhec.gov)
  • Low-density lipoprotein (LDL) cholesterol is bad cholesterol that can undergo peroxidation due to free radical damage and cause plaque formation in the coronary arteries. (medicinenet.com)
  • Having high triglyceride levels plus high LDL may increase the risk of plaque buildup in your arteries. (healthline.com)
  • This healthy type of cholesterol helps to remove LDL cholesterol - the "bad" type - from your arteries. (healthline.com)
  • Higher levels of LDL are associated with the buildup of dangerous plaque in the arteries which can lead to heart disease, heart attack, or stroke. (requestatest.com)
  • Oxidized LDL can cause inflammation in the blood vessels, increase the buildup of plaque in the arteries, and increase the risk or heart disease and events like a heart attack or stroke. (requestatest.com)
  • These LDL particles are modified by a number of mechanisms, including enzymatic degradation, aggregation and oxidation. (europa.eu)
  • In addition to trypsin, plasmin, thrombin, tryptase and matrix metalloprotease-2 each yielded E-LDL particles with high C1-activating efficiency, and the C1 activation extent was strictly dependent on cholesterol esterase treatment in all cases. (europa.eu)
  • Whereas treatment of E-LDL particles with human serum albumin reduced their free fatty acid content, both cholesterol and free fatty acids were decreased by methyl-beta cyclodextrin, both treatments resulting in a dose-dependent inhibition of the C1-activating ability of the particles. (europa.eu)
  • In view of these observations, it is tempting to hypothesize that, through its ability to bind fatty acids on E-LDL particles, C1q may prevent or control their proapoptotic effect. (europa.eu)
  • Lipoproteins are complex particles composed of multiple proteins, typically 80-100 proteins per particle (organized by a single apolipoprotein B for LDL and the larger particles). (wikipedia.org)
  • LDL particles are approximately 22 nm (0.00000087 in. (wikipedia.org)
  • Since LDL particles contain a variable and changing number of fatty acid molecules, there is a distribution of LDL particle mass and size. (wikipedia.org)
  • When LDL receptors bind LDL particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell. (wikipedia.org)
  • LDL can be grouped based on its size: large low density LDL particles are described as pattern A, and small high density LDL particles are pattern B. Pattern B has been associated by some with a higher risk for coronary heart disease. (wikipedia.org)
  • Pattern I, for intermediate, indicates that most LDL particles are very close in size to the normal gaps in the endothelium (26 nm). (wikipedia.org)
  • Cholesterol and other fats are transported through the blood stream in the form of round particles called lipoproteins. (choc.org)
  • LDL particle size plays a role in oxidation with smaller particles more likely to become oxidized. (requestatest.com)
  • However, for people with elevated Triglyceride levels, their LDL calculation may not be accurate. (requestatest.com)
  • The prevalence of type 2 diabetes among 25,000 patients with familial hypercholesterolemia (a genetic disorder characterized by high low-density lipoprotein [LDL] cholesterol levels) was significantly lower than among unaffected relatives, with the prevalence varying by the type of gene mutation, according to a study in the March 10 issue of JAMA. (news-medical.net)
  • With hypercholesterolemia, you either have too much LDL cholesterol or too little high-density lipoprotein (HDL) cholesterol in your blood. (healthline.com)
  • Hypercholesterolemia is above normal levels of LDL or total cholesterol in your blood. (healthline.com)
  • MANNHEIM, Germany - A novel drug that targets production of a liver protein involved in lipid metabolism appears to markedly reduce low-density lipoprotein (LDL) cholesterol levels for patients with homozygous familial hypercholesterolemia (HoFH), suggest results from the phase 2 GATEWAY trial. (medscape.com)
  • The aim of this study was to investigate whether consumption of a newly developed oat milk deprived of insoluble fiber would result in lower serum cholesterol and low-density lipoprotein (LDL) cholesterol levels in men with moderate hypercholesterolemia. (lu.se)
  • When a cell requires additional cholesterol (beyond its current internal HMGCoA production pathway), it synthesizes the necessary LDL receptors as well as PCSK9, a proprotein convertase that marks the LDL receptor for degradation. (wikipedia.org)
  • LDL receptors are inserted into the plasma membrane and diffuse freely until they associate with clathrin-coated pits. (wikipedia.org)
  • Vesicles containing LDL receptors bound to LDL are delivered to the endosome. (wikipedia.org)
  • In the presence of low pH, such as that found in the endosome, LDL receptors undergo a conformation change, releasing LDL. (wikipedia.org)
  • LDL receptors are typically returned to the plasma membrane, where they repeat this cycle. (wikipedia.org)
  • If LDL receptors bind to PCSK9, however, transport of LDL receptors is redirected to the lysosome, where they are degraded. (wikipedia.org)
  • Ng lipoproteins are taken up by two functionally significant low-density lipoprotein (LDL) receptors: the prototypic LDL receptor (LDLR) along with the LDL receptor-related protein 1 (LRP1). (nicotinic-receptor.com)
  • Plasminogen receptors promote lipoprotein(a) uptake by enhancing surface binding and facilitating macropinocytosis. (otago.ac.nz)
  • E-LDL is recognised by the C1q subunit of C1 and triggers direct C1 activation, suggesting that complement activation by E-LDL may play a crucial role in the pathogenesis of atherosclerosis. (europa.eu)
  • Lipoprotein oxidation has been implicated in the pathogenesis of atherosclerosis. (scienceopen.com)
  • To explore the involvement of tyrosyl radical, hydroxyl radical, and metal ions in atherosclerosis, we developed a highly sensitive and quantitative method for measuring levels of o, o'-dityrosine, o-tyrosine, and m-tyrosine in proteins, lipoproteins, and tissue, using stable isotope dilution gas chromatography-mass spectrometry. (scienceopen.com)
  • The detection of a selective increase of o,o'-dityrosine in LDL isolated from vascular lesions is consistent with the hypothesis that oxidative damage in human atherosclerosis is mediated in part by tyrosyl radical. (scienceopen.com)
  • Whereas most studies have demonstrated a strong association between lipoprotein (a) and the presence and severity of coronary heart disease, other groups have failed to observe such a relationship, which does question the importance of this particle in promoting atherosclerosis. (nih.gov)
  • Evidence from a study of human coronary atherosclerosis appears to demonstrate that the pathogenicity of lipoprotein (a) is modulated by concomitant LDL-cholesterol levels. (nih.gov)
  • Like other members of its class (the "statins"), simvastatin lowers total serum cholesterol and particularly low density lipoprotein (LDL) cholesterol concentrations, thereby reducing the risk of atherosclerosis and its complications - myocardial infarction and stroke. (nih.gov)
  • Moreover, the early stage of atherosclerosis is associated with increased levels of ox-LDL, oxidative stress, adhesion molecules and inflammatory cytokines in the vascular endothelium [ 6 - 8 ]. (biomedcentral.com)
  • In fact, a study suggests that ~50% of the cholesterol found in atherosclerotic plaque is derived from TRL-C even though, in most patients, TRL-C levels are much lower than calculated LDL-C. [ 8 ] Another area of confusion is that hypertriglyceridaemia is associated with a myriad of lipoprotein modifications and it is unclear which of these changes (if not all) are causal for atherosclerosis. (medscape.com)
  • For that reason, the most recent European Society of Cardiology and European Atherosclerosis Society guidelines no longer recommend specific cutoff points for LDL-C. (medscape.com)
  • To help answer that question, researchers at Western University's Robarts Research Institute have identified that an estrogen receptor, previously shown to regulate blood pressure in women, also plays an important role in regulating low-density lipoprotein (LDL) cholesterol levels. (news-medical.net)
  • An LDL (direct) test is typically ordered when a person has been shown to have high Triglyceride levels which can affect the accuracy of their LDL measurement in a standard Lipid Panel . (requestatest.com)
  • Applying these findings to LDL isolated from human atherosclerotic lesions, we detected a 100-fold increase in o,o'-dityrosine levels compared to those in circulating LDL. (scienceopen.com)
  • In striking contrast, levels of o-tyrosine and m-tyrosine were not elevated in LDL isolated from atherosclerotic tissue. (scienceopen.com)
  • High LDL levels cause plaque to build up in the blood vessels, narrowing them. (medicalnewstoday.com)
  • According to the National Heart, Lung, and Blood Institute (NHLBI) , high levels of LDL cholesterol usually do not cause symptoms. (medicalnewstoday.com)
  • The optimal levels of LDL cholesterol are less than 100 mg/dl, while HDL cholesterol levels should ideally be 60 mg/dl or higher. (medicalnewstoday.com)
  • Some drugs can increase levels of LDL cholesterol or decrease levels of HDL cholesterol. (medicalnewstoday.com)
  • People may inherit a tendency to have high levels of LDL cholesterol. (medicalnewstoday.com)
  • Signs of the condition include high levels of LDL cholesterol and total cholesterol. (medicalnewstoday.com)
  • As a consequence of its interaction with LDL, alternative strategies for treating high levels of lipoprotein (a) will be discussed. (nih.gov)
  • post-menopausal women with a higher serum FSH (≥78.3 IU/L) had higher serum TC and LDL-C levels than those with relatively lower FSH levels (40-78.3 IU/L), and ovariectomized mice had higher serum FSH and lipid levels and reduced hepatic LDL receptor expression. (nature.com)
  • Loci associated with increased risk for depression were also associated with increased risk of coronary artery disease and higher total cholesterol, low-density lipoprotein and c-reactive protein levels, while there was a mixed pattern of effect direction for the other risk factors. (plos.org)
  • High levels of "bad" LDL cholesterol cause plaque (fatty deposits) to build up in your blood vessels. (nih.gov)
  • A total of 54 Thais whose serum LDL levels ranged from 130 to 239 mg/dL at randomization, were enrolled and randomized into two groups. (tci-thaijo.org)
  • CONCLUSION: Among this population of hypercholesterolemic Thais, the daily replacement of an ordinary cup of coffee with a plant stanol mixed coffee reduced serum LDL levels by 12.77% demonstrating the effi cacy of the cholesterol-lowering ingredient in the new food matrix. (tci-thaijo.org)
  • We are currently studying the regulation of lipoprotein levels and composition to identify therapeutic targets for their manipulation with a particular interest in the Lp(a) and HDL lipoproteins which have opposing risk associations with heart disease. (otago.ac.nz)
  • Because HDL cholesterol plays an important role in getting rid of LDL, you want higher levels of HDL in your blood. (healthline.com)
  • A separate study found that, compared with placebo or statin monotherapy, evacetrapib as monotherapy or in combination with statins increased HDL-C levels and decreased LDL-C levels. (medscape.com)
  • Current guidelines recommend using statin therapy after CABG to keep LDL levels below 100 mg/dL. (medscape.com)
  • The current interim analysis showed that after 20 weeks, LDL cholesterol levels decreased by 48.1% and 44.0%, respectively, in the two groups. (medscape.com)
  • Mean LDL cholesterol levels in New York City and nationally were similar. (cdc.gov)
  • Despite advances in lowering total blood cholesterol, particularly throughout the 1980s (6,7), and the recent broad-scale use of medications targeting LDL cholesterol, control of lipid levels remains poor in the United States. (cdc.gov)
  • However, no study has examined LDL cholesterol levels by using a representative sample in New York City or in any exclusively urban setting. (cdc.gov)
  • To define high LDL levels, we used the National Cholesterol Education Program Adult Treatment Panel III (ATP III) guidelines, which provide thresholds for diagnosing and targets for lowering high LDL cholesterol on the basis of individual CHD risk (5,14). (cdc.gov)
  • 95% confidence interval (CI) 51.7 - 65.0) had dyslipidaemia, 16.3% (n=24/147) had low HDL-C levels, 53.8% (n=78/145) had high LDL-C levels and 14.9% (n=22/148) had raised TG levels. (who.int)
  • Compared with the control drink, intake of oat milk resulted in significantly lower serum total cholesterol (6, p = 0.005) and LDL cholesterol (6, p = 0.036) levels. (lu.se)
  • In addition, their prevalence of obesity, low high density lipoprotein (HDL), high low density lipoprotein (LDL), and high total cholesterol levels was higher relative to the general population. (cdc.gov)
  • The cholesterol content in these triglyceride-rich lipoproteins has been estimated by the Freidwald formula as approximately triglyceride levels divided by five, because these lipoproteins have ~60% triglyceride and 12% cholesterol (a 5:1 ratio). (medscape.com)
  • Although guidelines have historically focused on achieving specific levels of low-density lipoprotein cholesterol (LDL-C), there is increasing recognition that in many cases lower levels are progressively beneficial. (medscape.com)
  • Tujuan penelitian ini adalah untuk untuk mengetahui kandungan logam berat timbal (Pb) yang terdapat pada kerang darah (Anadara granosa) dan mengetahui kandungan LDL dan HDL pada kerang darah dari hasil tangkap nelayan di Pasar Ikan Brondong, Lamongan. (unair.ac.id)
  • Penelitian ini bertujuan untuk mengetahui adakah pengaruh pemberian ekstrak kulit jeruk lemon terhadap peningkatan kadar Low Density Lipoprotein (LDL) dan penurunan High Density Lipoprotein (HDL) pada tikus putih galur wistar (Rattus norvegicus) yang diberi diet tinggi lemak. (uwks.ac.id)
  • How to cite (IEEE): M. Sentosa, T. R. Saraswati, and S. Tana, "Kadar Low Density Lipoprotein (Ldl) Kuning Telur Puyuh Jepang (Coturnix coturnix japonica L.) setelah Pemberian Tepung Kunyit (Curcuma longa L.) pada Pakan," Buletin Anatomi dan Fisiologi , vol. 2, no. 1, pp. 94-98, Mar. 2017. (undip.ac.id)
  • How to cite (Vancouver): Sentosa M, Saraswati TR, Tana S. Kadar Low Density Lipoprotein (Ldl) Kuning Telur Puyuh Jepang (Coturnix coturnix japonica L.) setelah Pemberian Tepung Kunyit (Curcuma longa L.) pada Pakan. (undip.ac.id)
  • article{BAF1099, author = {Marco Sentosa and Tyas Saraswati and Silvana Tana}, title = {Kadar Low Density Lipoprotein (Ldl) Kuning Telur Puyuh Jepang (Coturnix coturnix japonica L.) setelah Pemberian Tepung Kunyit (Curcuma longa L.) pada Pakan}, journal = {Buletin Anatomi dan Fisiologi}, volume = {2}, number = {1}, year = {2017}, keywords = {}, abstract = { Puyuh merupakan komoditas peternakan dengan berbagai keunggulan, salah satunya adalah produksi telur untuk konsumsi. (undip.ac.id)
  • Tujuan dari penelitian ini adalah untuk mengetahui kadar LDL kuning telur pada puyuh Jepang ( Coturnix coturnix japonica L.) setelah pemberian suplemen serbuk kunyit pada pakan sebelum masak kelamin. (undip.ac.id)
  • Plant stanols dose-dependently decrease LDL-cholesterol concentra- tions, but not cholesterol-standardized fat-soluble anti oxidant concentrations, at intakes up to 9 g/d. (tci-thaijo.org)
  • These results suggest that Klotho can attenuate ox-LDL-induced oxidative stress in HUVECs through upregulating oxidative scavengers (SOD and NO) viaactivating the PI3K/Akt/eNOS pathway and depressing LOX-1expression. (biomedcentral.com)
  • Mass spectrometric quantification of markers for protein oxidation by tyrosyl radical, copper, and hydroxyl radical in low density lipoprotein isolated from human atherosclerotic plaques. (scienceopen.com)
  • In contrast, these observations do not support a role for free metal ions as catalysts of LDL oxidation in the artery wall. (scienceopen.com)
  • Pharmacotherapeutic strategies that affect the risk factor profile, such as the administration of statins for low-density lipoprotein (LDL) reduction or the administration of agents that alter atherosclerotic plaque, are of paramount importance. (medscape.com)
  • HDL and LDL are two types of lipoproteins.They are a combination of fat (lipid) and protein. (medlineplus.gov)
  • Lipoproteins are made of fat and protein. (medlineplus.gov)
  • Data on total cholesterol are provided in the Cholesterol - Total (P_TCHOL) file, and HDL-C data are provided in Cholesterol - High - Density Lipoprotein (P_HDL). (cdc.gov)
  • HDL, or high-density lipoprotein cholesterol, acts as the body's waste-disposal system in the blood. (wikihow.com)
  • There was no difference in serum cholesterol/high-density lipoprotein (HDL)-C and low-density lipoprotein (LDL)-C/HDL-C ratios between D-psicose group and other groups. (nih.gov)
  • Dr. Remaley's research has focused on the beneficial role of high-density lipoprotein (HDL), the so-called "good cholesterol. (nih.gov)
  • High-density lipoprotein (HDL), sometimes called "good" cholesterol. (nih.gov)
  • High-density lipoprotein (HDL) cholesterol is good cholesterol that clears LDL cholesterol from the blood and takes it back to the liver to break down. (medicinenet.com)
  • High-density lipoprotein (HDL) cholesterol is also known as "good" cholesterol. (healthline.com)
  • The concentration of high-density lipoprotein cholesterol was not significantly different after consumption of the two drinks. (lu.se)
  • Parameter utama yang diamati dalam penelitian ini adalah konsentrasi logam berat timbal (Pb), LDL dan HDL. (unair.ac.id)
  • Kesimpulan penelitian ini adalah pemberian suplemen serbuk kunyit dapat menurunkan kadar LDL kuning telur. (undip.ac.id)
  • A Prospective Randomized Trial for Reduction of Serum Low Density Lipoprotein (LDL) with Plant Stanol Ester Mixed in Coffee in a Hypercholesterolemic Thai Population. (tci-thaijo.org)
  • OBJECTIVE: To determine whether replacing ordinary coffee with coffee mixed with the plant stanol ester decreases the serum low density lipoprotein (LDL) level in moderately hypercholesterolemic Thais. (tci-thaijo.org)
  • The percentage of serum LDL reduction was measured at the end of the study. (tci-thaijo.org)
  • Incremental Reduction of Serum Total Cholesterol and Low-Density Lipoprotein Cholesterol With the Addition of Plant Stanol Ester-Containing Spread to Statin Therapy. (tci-thaijo.org)
  • It takes a village to do a good science" is a motto of Dr. Alan Remaley's team of the Lipoprotein Metabolism Laboratory. (nih.gov)
  • ANGPTL3 regulates lipoprotein metabolism by inhibiting lipoprotein and endothelial lipases. (medscape.com)
  • This strategy has been adopted globally primarily by recommending statin therapy to lower LDL-C. There is a general consensus that the lower the LDL-C, the better the clinical outcomes. (medscape.com)
  • There is increasing evidence that free fatty acids have the ability to trigger cell apoptosis and it has been shown that exposure of endothelial cells to E-LDL results in programmed cell death. (europa.eu)
  • The aim of this study is to investigatethe anti-oxidative activity of Klothoin ox-LDL-treated human umbilical vein endothelial cells (HUVECs). (biomedcentral.com)
  • Hasil penelitian review jurnal adanya pengaruh pemberian ekstrak kulit lemon terhadap peningkatan kadar LDL dan HDL dalam darah tikus putih jantan ( Rattus novergicus, L.) yang diberi diet tinggi lemak. (uwks.ac.id)
  • Telur puyuh memiliki kandungan gizi yang cukup tinggi, namun juga memiliki kadar Low Density Lipoprotein (LDL) yang tinggi. (undip.ac.id)
  • Hasil penelitian menunjukkan bahwa pemberian suplemen serbuk kunyit berbeda nyata terhadap kadar LDL kuning telur, namun berbeda tidak nyata terhadap konsumsi pakan, bobot telur, dan bobot kuning telur. (undip.ac.id)
  • Results- After a median follow-up of 5.3 years, the achieved LDL cholesterol was 66 (1.69 mmol/L) and 96 mg/dL (2.46 mmol/L) on average, respectively. (bvsalud.org)
  • An oxidized LDL test is typically ordered along with or as a follow up to a Lipid Panel Cholesterol Test . (requestatest.com)
  • LDL may decrease with acute illness, accident or surgery or increase during pregnancy. (requestatest.com)
  • Having too much LDL is linked to heart disease and stroke. (medlineplus.gov)
  • Dari hasil pemeriksaan kandungan Low Density Lipoprorein (LDL) yang terkandung dalam kerang darah (Anadara granosa) dari hasil tangkapan nelayan yaitu 28,6 mg/dL. (unair.ac.id)
  • On average, every 1% reduction in LDL cholesterol is matched by a 1% reduction in the likelihood of a major cardiac event (5). (cdc.gov)
  • The various approaches used in this study all concur in the conclusion that C1 binding to E-LDL involves recognition by C1q of the free fatty acids generated upon CEase treatment. (europa.eu)
  • A study published in the January/February 2015 issue of the Journal of Clinical Lipidology indicates corn oil significantly reduces cholesterol more than extra virgin olive oil with favorable changes in both total and low-density lipoprotein (LDL) cholesterol. (news-medical.net)
  • Prevalence of high total cholesterol and high LDL cholesterol remained virtually unchanged between 1988-1994 and 1999-2004 (8,9), and only one-fourth of US adults with elevated LDL cholesterol have their condition appropriately controlled (8). (cdc.gov)
  • Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein that transport all fat molecules around the body in extracellular water. (wikipedia.org)
  • Increased low density lipoprotein (LDL) and its oxidative form, oxidized low density lipoprotein (ox-LDL), inthe vascular sub-endothelium is characteristic of atherogenesis. (biomedcentral.com)
  • When incorporated into vesicles, the lipid fraction of E-LDL, but not of native LDL, triggered C1 activation, and activation correlated with the amount of free cholesterol released by cholesterol esterase. (europa.eu)
  • Each native LDL particle enables emulsification, i.e. surrounding the fatty acids being carried, enabling these fats to move around the body within the water outside cells. (wikipedia.org)
  • Increased oxidized low density lipoprotein (ox-LDL) in the sub-endothelium is the characteristic origin of atherogenesis. (biomedcentral.com)
  • The turnaround time for a LDL Cholesterol (direct) test is typically 1 business day. (requestatest.com)
  • A single LDL particle is about 220-275 angstroms in diameter, typically transporting 3,000 to 6,000 fat molecules per particle, and varying in size according to the number and mix of fat molecules contained within. (wikipedia.org)
  • Parameter yang diamati adalah LDL kuning telur, bobot kuning telur, bobot telur, dan konsumsi pakan. (undip.ac.id)
  • Some cholesterol medicines , including certain statins , can raise your HDL level, in addition to lowering your LDL level. (medlineplus.gov)