Abnormally high BLOOD GLUCOSE level.
Glucose in blood.
Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
Substances which lower blood glucose levels.
An antibiotic that is produced by Stretomyces achromogenes. It is used as an antineoplastic agent and to induce diabetes in experimental animals.
A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.
A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
Minor hemoglobin components of human erythrocytes designated A1a, A1b, and A1c. Hemoglobin A1c is most important since its sugar moiety is glucose covalently bound to the terminal amino acid of the beta chain. Since normal glycohemoglobin concentrations exclude marked blood glucose fluctuations over the preceding three to four weeks, the concentration of glycosylated hemoglobin A is a more reliable index of the blood sugar average over a long period of time.
The time frame after a meal or FOOD INTAKE.
Abstaining from all food.
Conditions or pathological processes associated with the disease of diabetes mellitus. Due to the impaired control of BLOOD GLUCOSE level in diabetic patients, pathological processes develop in numerous tissues and organs including the EYE, the KIDNEY, the BLOOD VESSELS, and the NERVE TISSUE.
Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration.
VASCULAR DISEASES that are associated with DIABETES MELLITUS.
The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).
Phlorhizin is a non-transportable glucose analog that inhibits the sodium-glucose cotransporter 1 (SGLT1) and aldohexose transporter (GLUT2), leading to reduced intestinal absorption and increased renal excretion of glucose, which is used in research to study glucose transport and diabetes-related processes.
Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.
A group of enzymes that catalyzes the conversion of ATP and D-glucose to ADP and D-glucose 6-phosphate. They are found in invertebrates and microorganisms, and are highly specific for glucose. (Enzyme Nomenclature, 1992) EC 2.7.1.2.
The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.
A pathological state in which BLOOD GLUCOSE level is less than approximately 140 mg/100 ml of PLASMA at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a GLUCOSE TOLERANCE TEST. This condition is seen frequently in DIABETES MELLITUS, but also occurs with other diseases and MALNUTRITION.
A serious complication of TYPE 2 DIABETES MELLITUS. It is characterized by extreme HYPERGLYCEMIA; DEHYDRATION; serum hyperosmolarity; and depressed consciousness leading to COMA in the absence of KETOSIS and ACIDOSIS.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Alloxan is a chemical compound, specifically an organic compound, that is used in scientific research to induce diabetes in laboratory animals by destroying their insulin-producing cells in the pancreas.
Two populations of Zucker rats have been cited in research--the "fatty" or obese and the lean. The "fatty" rat (Rattus norvegicus) appeared as a spontaneous mutant. The obese condition appears to be due to a single recessive gene.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The state of PREGNANCY in women with DIABETES MELLITUS. This does not include either symptomatic diabetes or GLUCOSE INTOLERANCE induced by pregnancy (DIABETES, GESTATIONAL) which resolves at the end of pregnancy.
Elements of limited time intervals, contributing to particular results or situations.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.
An autosomal recessive metabolic disorder caused by deficiencies in the mitochondrial GLYCINE cleavage system.
A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.
Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as CHOREATIC DISORDERS. Chorea is also a frequent manifestation of BASAL GANGLIA DISEASES.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Products derived from the nonenzymatic reaction of GLUCOSE and PROTEINS in vivo that exhibit a yellow-brown pigmentation and an ability to participate in protein-protein cross-linking. These substances are involved in biological processes relating to protein turnover and it is believed that their excessive accumulation contributes to the chronic complications of DIABETES MELLITUS.
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.
FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)
A disease or state in which death is possible or imminent.
The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.
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.
An amino sugar formed when glucose non-enzymatically reacts with the N-terminal amino group of proteins. The fructose moiety is derived from glucose by the "classical" Amadori rearrangement.
Disease having a short and relatively severe course.
Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
A glucose transport facilitator that is expressed primarily in PANCREATIC BETA CELLS; LIVER; and KIDNEYS. It may function as a GLUCOSE sensor to regulate INSULIN release and glucose HOMEOSTASIS.
An inhibitor of ALPHA-GLUCOSIDASES that retards the digestion and absorption of DIETARY CARBOHYDRATES in the SMALL INTESTINE.
The release of GLUCOSE from GLYCOGEN by GLYCOGEN PHOSPHORYLASE (phosphorolysis). The released glucose-1-phosphate is then converted to GLUCOSE-6-PHOSPHATE by PHOSPHOGLUCOMUTASE before entering GLYCOLYSIS. Glycogenolysis is stimulated by GLUCAGON or EPINEPHRINE via the activation of PHOSPHORYLASE KINASE.
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.
Conditions with excess LIPIDS in the blood.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Hexosamines are amino sugars that are formed by the substitution of an amino group for a hydroxyl group in a hexose sugar, playing crucial roles in various biological processes such as glycoprotein synthesis and protein folding.
Glycogen is a multibranched polysaccharide of glucose serving as the primary form of energy storage in animals, fungi, and bacteria, stored mainly in liver and muscle tissues. (Two sentences combined as per your request)
Diabetes mellitus induced by PREGNANCY but resolved at the end of pregnancy. It does not include previously diagnosed diabetics who become pregnant (PREGNANCY IN DIABETICS). Gestational diabetes usually develops in late pregnancy when insulin antagonistic hormones peaks leading to INSULIN RESISTANCE; GLUCOSE INTOLERANCE; and HYPERGLYCEMIA.
An enzyme that catalyzes the conversion of D-glucose 6-phosphate and water to D-glucose and orthophosphate. EC 3.1.3.9.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Glycogen stored in the liver. (Dorland, 28th ed)
The processes whereby the internal environment of an organism tends to remain balanced and stable.
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.
An enzyme that catalyzes reversibly the oxidation of an aldose to an alditol. It possesses broad specificity for many aldoses. EC 1.1.1.21.
A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
A state of unconsciousness as a complication of diabetes mellitus. It occurs in cases of extreme HYPERGLYCEMIA or extreme HYPOGLYCEMIA as a complication of INSULIN therapy.
A pancreatic polypeptide of about 110 amino acids, depending on the species, that is the precursor of insulin. Proinsulin, produced by the PANCREATIC BETA CELLS, is comprised sequentially of the N-terminal B-chain, the proteolytically removable connecting C-peptide, and the C-terminal A-chain. It also contains three disulfide bonds, two between A-chain and B-chain. After cleavage at two locations, insulin and C-peptide are the secreted products. Intact proinsulin with low bioactivity also is secreted in small amounts.
A sodium-glucose transporter that is expressed in the luminal membrane of the PROXIMAL KIDNEY TUBULES.
A type of pancreatic cell representing about 5-20% of the islet cells. Alpha cells secrete GLUCAGON.
A 14-amino acid peptide named for its ability to inhibit pituitary GROWTH HORMONE release, also called somatotropin release-inhibiting factor. It is expressed in the central and peripheral nervous systems, the gut, and other organs. SRIF can also inhibit the release of THYROID-STIMULATING HORMONE; PROLACTIN; INSULIN; and GLUCAGON besides acting as a neurotransmitter and neuromodulator. In a number of species including humans, there is an additional form of somatostatin, SRIF-28 with a 14-amino acid extension at the N-terminal.
Portable or implantable devices for infusion of insulin. Includes open-loop systems which may be patient-operated or controlled by a pre-set program and are designed for constant delivery of small quantities of insulin, increased during food ingestion, and closed-loop systems which deliver quantities of insulin automatically based on an electronic glucose sensor.
A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)
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.
A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications.
Self evaluation of whole blood glucose levels outside the clinical laboratory. A digital or battery-operated reflectance meter may be used. It has wide application in controlling unstable insulin-dependent diabetes.
Cell surface receptors that bind glucagon with high affinity and trigger intracellular changes which influence the behavior of cells. Activation of glucagon receptors causes a variety of effects; the best understood is the initiation of a complex enzymatic cascade in the liver which ultimately increases the availability of glucose to body organs.
Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.

Accelerated intimal hyperplasia and increased endogenous inhibitors for NO synthesis in rabbits with alloxan-induced hyperglycaemia. (1/3915)

1. We examined whether endogenous inhibitors of NO synthesis are involved in the augmentation of intimal hyperplasia in rabbits with hyperglycaemia induced by alloxan. 2. Four weeks after the endothelial denudation of carotid artery which had been performed 12 weeks after alloxan, the intimal hyperplasia was greatly augmented with hyperglycaemia. The degree of hyperplasia was assessed using three different parameters of histopathological findings as well as changes in luminal area and intima: media ratio. 3. There were positive and significant correlations between intima:media ratio, plasma glucose, and concentrations of N(G)-monomethyl-L-arginine (L-NMMA) and N(G), N(G)-dimethyl-L-arginine (ADMA) in endothelial cells, that is, the intima:media ratio became greater as plasma glucose and endothelial L-NMMA and ADMA were increased. Furthermore, endothelial L-NMMA and ADMA were increased in proportion to the increase in plasma glucose. 4. In contrast, there were inverse and significant correlations between cyclic GMP production by carotid artery strips with endothelium and plasma glucose, between cyclic GMP production and endothelial L-NMMA and ADMA, and between the intima:media ratio and cyclic GMP production. 5. Exogenously applied L-NMMA and ADMA inhibited cyclic GMP production in a concentration-dependent manner. IC50 values were determined to be 12.1 microM for the former and 26.2 microM for the latter. The cyclic GMP production was abolished after the deliberate removal of endothelium from the artery strips. 6. These results suggest that the augmentation of intimal hyperplasia with hyperglycaemia is closely related to increased accumulation of L-NMMA and ADMA with hyperglycaemia, which would result in an accelerated reduction in NO production/release by endothelial cells.  (+info)

Effect of hyperglycemia-hyperinsulinemia on whole body and regional fatty acid metabolism. (2/3915)

The effects of combined hyperglycemia-hyperinsulinemia on whole body, splanchnic, and leg fatty acid metabolism were determined in five volunteers. Catheters were placed in a femoral artery and vein and a hepatic vein. U-13C-labeled fatty acids were infused, once in the basal state and, on a different occasion, during infusion of dextrose (clamp; arterial glucose 8.8 +/- 0.5 mmol/l). Lipids and heparin were infused together with the dextrose to maintain plasma fatty acid concentrations at basal levels. Fatty acid availability in plasma and fatty acid uptake across the splanchnic region and the leg were similar during the basal and clamp experiments. Dextrose infusion decreased fatty acid oxidation by 51.8% (whole body), 47.4% (splanchnic), and 64.3% (leg). Similarly, the percent fatty acid uptake oxidized decreased at the whole body level (53 to 29%), across the splanchnic region (30 to 13%), and in the leg (48 to 22%) during the clamp. We conclude that, in healthy men, combined hyperglycemia-hyperinsulinemia inhibits fatty acid oxidation to a similar extent at the whole body level, across the leg, and across the splanchnic region, even when fatty acid availability is constant.  (+info)

Effects of duodenal distension on antropyloroduodenal pressures and perception are modified by hyperglycemia. (3/3915)

Marked hyperglycemia (blood glucose approximately 15 mmol/l) affects gastrointestinal motor function and modulates the perception of gastrointestinal sensations. The aims of this study were to evaluate the effects of mild hyperglycemia on the perception of, and motor responses to, duodenal distension. Paired studies were done in nine healthy volunteers, during euglycemia ( approximately 4 mmol/l) and mild hyperglycemia ( approximately 10 mmol/l), in randomized order, using a crossover design. Antropyloroduodenal pressures were recorded with a manometric, sleeve-side hole assembly, and proximal duodenal distensions were performed with a flaccid bag. Intrabag volumes were increased at 4-ml increments from 12 to 48 ml, each distension lasting for 2.5 min and separated by 10 min. Perception of the distensions and sensations of fullness, nausea, and hunger were evaluated. Perceptions of distension (P < 0.001) and fullness (P < 0.05) were greater and hunger less (P < 0.001) during hyperglycemia compared with euglycemia. Proximal duodenal distension stimulated pyloric tone (P < 0.01), isolated pyloric pressure waves (P < 0.01), and duodenal pressure waves (P < 0.01). Compared with euglycemia, hyperglycemia was associated with increases in pyloric tone (P < 0.001), the frequency (P < 0.05) and amplitude (P < 0.01) of isolated pyloric pressure waves, and the frequency of duodenal pressure waves (P < 0.001) in response to duodenal distension. Duodenal compliance was less (P < 0.05) during hyperglycemia compared with euglycemia, but this did not account for the effects of hyperglycemia on perception. We conclude that both the perception of, and stimulation of pyloric and duodenal pressures by, duodenal distension are increased by mild hyperglycemia. These observations are consistent with the concept that the blood glucose concentration plays a role in the regulation of gastrointestinal motility and sensation.  (+info)

Time-dependent and tissue-specific effects of circulating glucose on fetal ovine glucose transporters. (4/3915)

To determine the cellular adaptations to fetal hyperglycemia and hypoglycemia, we examined the time-dependent effects on basal (GLUT-1 and GLUT-3) and insulin-responsive (GLUT-4) glucose transporter proteins by quantitative Western blot analysis in fetal ovine insulin-insensitive (brain and liver) and insulin-sensitive (myocardium, skeletal muscle, and adipose) tissues. Maternal glucose infusions causing fetal hyperglycemia resulted in a transient 30% increase in brain GLUT-1 but not GLUT-3 levels and a decline in liver and adipose GLUT-1 and myocardial and skeletal muscle GLUT-1 and GLUT-4 levels compared with gestational age-matched controls. Maternal insulin infusions leading to fetal hypoglycemia caused a decline in brain GLUT-3, an increase in brain GLUT-1, and a subsequent decline in liver GLUT-1, with no significant change in insulin-sensitive myocardium, skeletal muscle, and adipose tissue GLUT-1 or GLUT-4 concentrations, compared with gestational age-matched sham controls. We conclude that fetal glucose transporters are subject to a time-dependent and tissue- and isoform-specific differential regulation in response to altered circulating glucose and/or insulin concentrations. These cellular adaptations in GLUT-1 (and GLUT-3) are geared toward protecting the conceptus from perturbations in substrate availability, and the adaptations in GLUT-4 are geared toward development of fetal insulin resistance.  (+info)

Brain-derived neurotrophic factor improves blood glucose control and alleviates fasting hyperglycemia in C57BLKS-Lepr(db)/lepr(db) mice. (5/3915)

Systemic administration of brain-derived neurotrophic factor (BDNF) decreases nonfasted blood glucose in obese, non-insulin-dependent diabetic C57BLKS-Lepr(db)/lepr(db) (db/db) mice, with a concomitant decrease in body weight. By measuring percent HbA1c in BDNF-treated and pair-fed animals, we show that the effects of BDNF on nonfasted blood glucose levels are not caused by decreased food intake but reflect a significant improvement in blood glucose control. Furthermore, once established, this effect can persist for weeks after cessation of BDNF treatment. Oral glucose tolerance tests were performed to examine the effects of BDNF on blood glucose control in the fasted state and after an oral glucose challenge. BDNF treatment normalized fasting blood glucose from initially hyperglycemic levels and also showed evidence for beneficial, although less marked, effects on the ability to remove exogenous glucose from blood. One means to lower fasting blood glucose is to reduce the glucose output of peripheral tissues that normally play a part in the maintenance of fasting hyperglycemia. Because the liver is the major endogenous source of glucose in blood during fasting, and because hepatic weight and glucose output are increased in type 2 diabetes, we evaluated the effects of BDNF on liver tissue. BDNF reduced the hepatomegaly present in db/db mice, in association with reduced liver glycogen and reduced liver enzyme activity in serum, supporting the possible involvement of liver tissue in the mechanism of action for BDNF.  (+info)

Hyperglycemia inhibits insulin activation of Akt/protein kinase B but not phosphatidylinositol 3-kinase in rat skeletal muscle. (6/3915)

Sustained hyperglycemia impairs insulin-stimulated glucose utilization in the skeletal muscle of both humans and experimental animals--a phenomenon referred to clinically as glucose toxicity. To study how this occurs, a model was developed in which hyperglycemia produces insulin resistance in vitro. Rat extensor digitorum longus muscles were preincubated for 4 h in Krebs-Henseleit solution containing glucose or glucose + insulin at various concentrations, after which insulin action was studied. Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose incorporation into lipid and its oxidation to CO2 were marginally diminished, if at all. The alterations of glycogen synthesis and 2-DG uptake were first evident after 1 h and were maximal after 2 h of preincubation; they were not observed in muscles preincubated with 25 mmol/l glucose + insulin for 5 min. Preincubation for 4 h with 25 mmol/l glucose in the absence of insulin produced a similar although somewhat smaller decrease in insulin-stimulated glycogen synthesis; however, it did not alter 2-DG uptake, glucose oxidation to CO2, or incorporation into lipids. Studies of insulin signaling in the latter muscles revealed that activation of Akt/protein kinase B (PKB) was diminished by 60%, compared with that of muscles preincubated in a glucose-free medium; whereas activation of phosphatidylinositol (PI) 3-kinase, an upstream regulator of Akt/PKB in the insulin-signaling cascade, and of mitogen-activated protein (MAP) kinase, a parallel signal, was unaffected. Immunoblots demonstrated that this was not due to a change in Akt/PKB abundance. The results indicate that hyperglycemia-induced insulin resistance can be studied in rat skeletal muscle in vitro. They suggest that impairment of insulin action in these muscles is related to inhibition of Akt/PKB by events that do not affect PI 3-kinase.  (+info)

Hyperglycemia and focal brain ischemia. (7/3915)

The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF.  (+info)

Renal changes on hyperglycemia and angiotensin-converting enzyme in type 1 diabetes. (8/3915)

Hyperglycemia causes capillary vasodilation and high glomerular capillary hydraulic pressure, which lead to glomerulosclerosis and hypertension in type 1 diabetic subjects. The insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene can modulate risk of nephropathy due to hyperglycemia, and the II genotype (producing low plasma ACE concentrations and probably reduced renal angiotensin II generation and kinin inactivation) may protect against diabetic nephropathy. We tested the possible interaction between ACE I/D polymorphism and uncontrolled type 1 diabetes by measuring glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) during normoglycemia ( approximately 5 mmol/L) and hyperglycemia ( approximately 15 mmol/L) in 9 normoalbuminuric, normotensive type 1 diabetic subjects with the II genotype and 18 matched controls with the ID or DD genotype. Baseline GFR (145+/-22 mL/min per 1.73 m2) and ERPF (636+/-69 mL/min per 1.73 m2) of II subjects declined by 8+/-10% and 10+/-9%, respectively, during hyperglycemia; whereas baseline GFR (138+/-16 mL/min per 1.73 m2) and ERPF (607+/-93 mL/min per 1.73 m2) increased by 4+/-7% and 6+/-11%, respectively, in ID and DD subjects (II versus ID or DD subjects: P=0.0007 and P=0.0005, for GFR and ERPF, respectively). The changes in renal hemodynamics of subjects carrying 1 or 2 D alleles were compatible, with a mainly preglomerular vasodilation induced by hyperglycemia, proportional to plasma ACE concentration (P=0.024); this was not observed in subjects with the II genotype. Thus, type 1 diabetic individuals with the II genotype are resistant to glomerular changes induced by hyperglycemia, providing a basis for their reduced risk of nephropathy.  (+info)

Hyperglycemia is a medical term that refers to an abnormally high level of glucose (sugar) in the blood. Fasting hyperglycemia is defined as a fasting blood glucose level greater than or equal to 126 mg/dL (milligrams per deciliter) on two separate occasions. Alternatively, a random blood glucose level greater than or equal to 200 mg/dL in combination with symptoms of hyperglycemia (such as increased thirst, frequent urination, blurred vision, and fatigue) can also indicate hyperglycemia.

Hyperglycemia is often associated with diabetes mellitus, a chronic metabolic disorder characterized by high blood glucose levels due to insulin resistance or insufficient insulin production. However, hyperglycemia can also occur in other conditions such as stress, surgery, infection, certain medications, and hormonal imbalances.

Prolonged or untreated hyperglycemia can lead to serious complications such as diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and long-term damage to various organs such as the eyes, kidneys, nerves, and blood vessels. Therefore, it is essential to monitor blood glucose levels regularly and maintain them within normal ranges through proper diet, exercise, medication, and lifestyle modifications.

Blood glucose, also known as blood sugar, is the concentration of glucose in the blood. Glucose is a simple sugar that serves as the main source of energy for the body's cells. It is carried to each cell through the bloodstream and is absorbed into the cells with the help of insulin, a hormone produced by the pancreas.

The normal range for blood glucose levels in humans is typically between 70 and 130 milligrams per deciliter (mg/dL) when fasting, and less than 180 mg/dL after meals. Levels that are consistently higher than this may indicate diabetes or other metabolic disorders.

Blood glucose levels can be measured through a variety of methods, including fingerstick blood tests, continuous glucose monitoring systems, and laboratory tests. Regular monitoring of blood glucose levels is important for people with diabetes to help manage their condition and prevent complications.

I couldn't find a medical definition specifically for "Diabetes Mellitus, Experimental." However, I can provide you with information about experimental diabetes research and its relevance to understanding the disease.

Experimental diabetes models are used in biomedical research to study the pathophysiology of diabetes mellitus and to test potential therapies or treatments. These models can be broadly categorized into two types: chemically-induced and genetically modified.

1. Chemically-induced diabetes models: These involve administering chemicals, such as alloxan or streptozotocin, to animals (commonly mice or rats) to destroy their pancreatic β-cells, which produce insulin. This results in hyperglycemia and symptoms similar to those seen in type 1 diabetes in humans.
2. Genetically modified diabetes models: These involve altering the genes of animals (commonly mice) to create a diabetes phenotype. Examples include non-obese diabetic (NOD) mice, which develop an autoimmune form of diabetes similar to human type 1 diabetes, and various strains of obese mice with insulin resistance, such as ob/ob or db/db mice, which model aspects of type 2 diabetes.

These experimental models help researchers better understand the mechanisms behind diabetes development and progression, identify new therapeutic targets, and test potential treatments before moving on to human clinical trials. However, it's essential to recognize that these models may not fully replicate all aspects of human diabetes, so findings from animal studies should be interpreted with caution.

Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.

Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.

Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.

In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.

Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.

Diabetes Mellitus, Type 2 is a metabolic disorder characterized by high blood glucose (or sugar) levels resulting from the body's inability to produce sufficient amounts of insulin or effectively use the insulin it produces. This form of diabetes usually develops gradually over several years and is often associated with older age, obesity, physical inactivity, family history of diabetes, and certain ethnicities.

In Type 2 diabetes, the body's cells become resistant to insulin, meaning they don't respond properly to the hormone. As a result, the pancreas produces more insulin to help glucose enter the cells. Over time, the pancreas can't keep up with the increased demand, leading to high blood glucose levels and diabetes.

Type 2 diabetes is managed through lifestyle modifications such as weight loss, regular exercise, and a healthy diet. Medications, including insulin therapy, may also be necessary to control blood glucose levels and prevent long-term complications associated with the disease, such as heart disease, nerve damage, kidney damage, and vision loss.

Hypoglycemic agents are a class of medications that are used to lower blood glucose levels in the treatment of diabetes mellitus. These medications work by increasing insulin sensitivity, stimulating insulin release from the pancreas, or inhibiting glucose production in the liver. Examples of hypoglycemic agents include sulfonylureas, meglitinides, biguanides, thiazolidinediones, DPP-4 inhibitors, SGLT2 inhibitors, and GLP-1 receptor agonists. It's important to note that the term "hypoglycemic" refers to a condition of abnormally low blood glucose levels, but in this context, the term is used to describe agents that are used to treat high blood glucose levels (hyperglycemia) associated with diabetes.

Streptozocin is an antibiotic and antineoplastic agent, which is primarily used in the treatment of metastatic pancreatic islet cell carcinoma (a type of pancreatic cancer). It is a naturally occurring compound produced by the bacterium Streptomyces achromogenes.

Medically, streptozocin is classified as an alkylating agent due to its ability to interact with DNA and RNA, disrupting the growth and multiplication of malignant cells. However, it can also have adverse effects on non-cancerous cells, particularly in the kidneys and pancreas, leading to potential side effects such as nephrotoxicity (kidney damage) and hyperglycemia (high blood sugar).

It is essential that streptozocin be administered under the supervision of a healthcare professional, who can monitor its effectiveness and potential side effects. The drug is typically given through intravenous infusion, with the dosage and duration tailored to individual patient needs and treatment responses.

A Glucose Tolerance Test (GTT) is a medical test used to diagnose prediabetes, type 2 diabetes, and gestational diabetes. It measures how well your body is able to process glucose, which is a type of sugar.

During the test, you will be asked to fast (not eat or drink anything except water) for at least eight hours before the test. Then, a healthcare professional will take a blood sample to measure your fasting blood sugar level. After that, you will be given a sugary drink containing a specific amount of glucose. Your blood sugar levels will be measured again after two hours and sometimes also after one hour.

The results of the test will indicate how well your body is able to process the glucose and whether you have normal, impaired, or diabetic glucose tolerance. If your blood sugar levels are higher than normal but not high enough to be diagnosed with diabetes, you may have prediabetes, which means that you are at increased risk of developing type 2 diabetes in the future.

It is important to note that a Glucose Tolerance Test should be performed under the supervision of a healthcare professional, as high blood sugar levels can be dangerous if not properly managed.

Diabetes Mellitus is a chronic metabolic disorder characterized by elevated levels of glucose in the blood (hyperglycemia) due to absolute or relative deficiency in insulin secretion and/or insulin action. There are two main types: Type 1 diabetes, which results from the autoimmune destruction of pancreatic beta cells leading to insulin deficiency, and Type 2 diabetes, which is associated with insulin resistance and relative insulin deficiency.

Type 1 diabetes typically presents in childhood or young adulthood, while Type 2 diabetes tends to occur later in life, often in association with obesity and physical inactivity. Both types of diabetes can lead to long-term complications such as damage to the eyes, kidneys, nerves, and cardiovascular system if left untreated or not well controlled.

The diagnosis of diabetes is usually made based on fasting plasma glucose levels, oral glucose tolerance tests, or hemoglobin A1c (HbA1c) levels. Treatment typically involves lifestyle modifications such as diet and exercise, along with medications to lower blood glucose levels and manage associated conditions.

Diabetes Mellitus, Type 1 is a chronic autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas, leading to an absolute deficiency of insulin. This results in an inability to regulate blood glucose levels, causing hyperglycemia (high blood sugar). Type 1 diabetes typically presents in childhood or early adulthood, although it can develop at any age. It is usually managed with regular insulin injections or the use of an insulin pump, along with monitoring of blood glucose levels and adjustments to diet and physical activity. Uncontrolled type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, blindness, and cardiovascular disease.

Hypoglycemia is a medical condition characterized by an abnormally low level of glucose (sugar) in the blood. Generally, hypoglycemia is defined as a blood glucose level below 70 mg/dL (3.9 mmol/L), although symptoms may not occur until the blood sugar level falls below 55 mg/dL (3.0 mmol/L).

Hypoglycemia can occur in people with diabetes who are taking insulin or medications that increase insulin production, as well as those with certain medical conditions such as hormone deficiencies, severe liver illnesses, or disorders of the adrenal glands. Symptoms of hypoglycemia include sweating, shaking, confusion, rapid heartbeat, and in severe cases, loss of consciousness or seizures.

Hypoglycemia is typically treated by consuming fast-acting carbohydrates such as fruit juice, candy, or glucose tablets to rapidly raise blood sugar levels. If left untreated, hypoglycemia can lead to serious complications, including brain damage and even death.

The Islets of Langerhans are clusters of specialized cells within the pancreas, an organ located behind the stomach. These islets are named after Paul Langerhans, who first identified them in 1869. They constitute around 1-2% of the total mass of the pancreas and are distributed throughout its substance.

The Islets of Langerhans contain several types of cells, including:

1. Alpha (α) cells: These produce and release glucagon, a hormone that helps to regulate blood sugar levels by promoting the conversion of glycogen to glucose in the liver when blood sugar levels are low.
2. Beta (β) cells: These produce and release insulin, a hormone that promotes the uptake and utilization of glucose by cells throughout the body, thereby lowering blood sugar levels.
3. Delta (δ) cells: These produce and release somatostatin, a hormone that inhibits the release of both insulin and glucagon and helps regulate their secretion in response to changing blood sugar levels.
4. PP cells (gamma or γ cells): These produce and release pancreatic polypeptide, which plays a role in regulating digestive enzyme secretion and gastrointestinal motility.

Dysfunction of the Islets of Langerhans can lead to various endocrine disorders, such as diabetes mellitus, where insulin-producing beta cells are damaged or destroyed, leading to impaired blood sugar regulation.

Hyperinsulinism is a medical condition characterized by an excess production and release of insulin from the pancreas. Insulin is a hormone that helps regulate blood sugar levels by allowing cells in the body to take in sugar (glucose) for energy or storage. In hyperinsulinism, the increased insulin levels can cause low blood sugar (hypoglycemia), which can lead to symptoms such as sweating, shaking, confusion, and in severe cases, seizures or loss of consciousness.

There are several types of hyperinsulinism, including congenital forms that are present at birth and acquired forms that develop later in life. Congenital hyperinsulinism is often caused by genetic mutations that affect the way insulin is produced or released from the pancreas. Acquired hyperinsulinism can be caused by factors such as certain medications, hormonal disorders, or tumors of the pancreas.

Treatment for hyperinsulinism depends on the underlying cause and severity of the condition. Treatment options may include dietary changes, medication to reduce insulin secretion, or surgery to remove part or all of the pancreas.

Glucagon is a hormone produced by the alpha cells of the pancreas. Its main function is to regulate glucose levels in the blood by stimulating the liver to convert stored glycogen into glucose, which can then be released into the bloodstream. This process helps to raise blood sugar levels when they are too low, such as during hypoglycemia.

Glucagon is a 29-amino acid polypeptide that is derived from the preproglucagon protein. It works by binding to glucagon receptors on liver cells, which triggers a series of intracellular signaling events that lead to the activation of enzymes involved in glycogen breakdown.

In addition to its role in glucose regulation, glucagon has also been shown to have other physiological effects, such as promoting lipolysis (the breakdown of fat) and inhibiting gastric acid secretion. Glucagon is often used clinically in the treatment of hypoglycemia, as well as in diagnostic tests to assess pancreatic function.

Insulin resistance is a condition in which the body's cells become less responsive to insulin, a hormone produced by the pancreas that regulates blood sugar levels. In response to this decreased sensitivity, the pancreas produces more insulin to help glucose enter the cells. However, over time, the pancreas may not be able to keep up with the increased demand for insulin, leading to high levels of glucose in the blood and potentially resulting in type 2 diabetes, prediabetes, or other health issues such as metabolic syndrome, cardiovascular disease, and non-alcoholic fatty liver disease. Insulin resistance is often associated with obesity, physical inactivity, and genetic factors.

Insulin-secreting cells, also known as beta cells, are a type of cell found in the pancreas. They are responsible for producing and releasing insulin, a hormone that regulates blood glucose levels by allowing cells in the body to take in glucose from the bloodstream. Insulin-secreting cells are clustered together in the pancreatic islets, along with other types of cells that produce other hormones such as glucagon and somatostatin. In people with diabetes, these cells may not function properly, leading to an impaired ability to regulate blood sugar levels.

Glycosylated Hemoglobin A, also known as Hemoglobin A1c or HbA1c, is a form of hemoglobin that is bound to glucose. It is formed in a non-enzymatic glycation reaction with glucose in the blood. The amount of this hemoglobin present in the blood is proportional to the average plasma glucose concentration over the previous 8-12 weeks, making it a useful indicator for monitoring long-term blood glucose control in people with diabetes mellitus.

In other words, HbA1c reflects the integrated effects of glucose regulation over time and is an important clinical marker for assessing glycemic control and risk of diabetic complications. The normal range for HbA1c in individuals without diabetes is typically less than 5.7%, while a value greater than 6.5% is indicative of diabetes.

The postprandial period is the time frame following a meal, during which the body is engaged in the process of digestion, absorption, and assimilation of nutrients. In a medical context, this term generally refers to the few hours after eating when the body is responding to the ingested food, particularly in terms of changes in metabolism and insulin levels.

The postprandial period can be of specific interest in the study and management of conditions such as diabetes, where understanding how the body handles glucose during this time can inform treatment decisions and strategies for maintaining healthy blood sugar levels.

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.

Diabetes complications refer to a range of health issues that can develop as a result of poorly managed diabetes over time. These complications can affect various parts of the body and can be classified into two main categories: macrovascular and microvascular.

Macrovascular complications include:

* Cardiovascular disease (CVD): People with diabetes are at an increased risk of developing CVD, including coronary artery disease, peripheral artery disease, and stroke.
* Peripheral arterial disease (PAD): This condition affects the blood vessels that supply oxygen and nutrients to the limbs, particularly the legs. PAD can cause pain, numbness, or weakness in the legs and may increase the risk of amputation.

Microvascular complications include:

* Diabetic neuropathy: This is a type of nerve damage that can occur due to prolonged high blood sugar levels. It commonly affects the feet and legs, causing symptoms such as numbness, tingling, or pain.
* Diabetic retinopathy: This condition affects the blood vessels in the eye and can cause vision loss or blindness if left untreated.
* Diabetic nephropathy: This is a type of kidney damage that can occur due to diabetes. It can lead to kidney failure if not managed properly.

Other complications of diabetes include:

* Increased risk of infections, particularly skin and urinary tract infections.
* Slow healing of wounds, which can increase the risk of infection and amputation.
* Gum disease and other oral health problems.
* Hearing impairment.
* Sexual dysfunction.

Preventing or managing diabetes complications involves maintaining good blood sugar control, regular monitoring of blood glucose levels, following a healthy lifestyle, and receiving routine medical care.

The glucose clamp technique is a method used in medical research, particularly in the study of glucose metabolism and insulin action. It's a controlled procedure that aims to maintain a steady state of plasma glucose concentration in an individual for a specific period.

In this technique, a continuous infusion of glucose is administered intravenously at a variable rate to balance the amount of glucose being removed from the circulation (for example, by insulin-stimulated uptake in muscle and fat tissue). This creates a "clamp" of stable plasma glucose concentration.

The rate of glucose infusion is adjusted according to frequent measurements of blood glucose levels, typically every 5 to 10 minutes, to keep the glucose level constant. The glucose clamp technique allows researchers to study how different factors, such as various doses of insulin or other drugs, affect glucose metabolism under standardized conditions.

There are two primary types of glucose clamps: the hyperglycemic clamp and the euglycemic clamp. The former aims to raise and maintain plasma glucose at a higher-than-normal level, while the latter maintains plasma glucose at a normal, euglycemic level.

Diabetic angiopathies refer to a group of vascular complications that occur due to diabetes mellitus. Prolonged exposure to high blood sugar levels can damage the blood vessels, leading to various types of angiopathies such as:

1. Diabetic retinopathy: This is a condition where the small blood vessels in the retina get damaged due to diabetes, leading to vision loss or blindness if left untreated.
2. Diabetic nephropathy: In this condition, the kidneys' glomeruli (the filtering units) become damaged due to diabetes, leading to protein leakage and eventually kidney failure if not managed properly.
3. Diabetic neuropathy: This is a type of nerve damage caused by diabetes that can affect various parts of the body, including the legs, feet, and hands, causing numbness, tingling, or pain.
4. Diabetic cardiomyopathy: This is a condition where the heart muscle becomes damaged due to diabetes, leading to heart failure.
5. Diabetic peripheral arterial disease (PAD): In this condition, the blood vessels that supply the legs and feet become narrowed or blocked due to diabetes, leading to pain, cramping, or even gangrene in severe cases.

Overall, diabetic angiopathies are serious complications of diabetes that can significantly impact a person's quality of life and overall health. Therefore, it is crucial for individuals with diabetes to manage their blood sugar levels effectively and undergo regular check-ups to detect any early signs of these complications.

Glycosuria is a medical term that refers to the presence of glucose in the urine. Under normal circumstances, the kidneys are able to reabsorb all of the filtered glucose back into the bloodstream. However, when the blood glucose levels become excessively high, such as in uncontrolled diabetes mellitus, the kidneys may not be able to reabsorb all of the glucose, and some of it will spill over into the urine.

Glycosuria can also occur in other conditions that affect glucose metabolism or renal function, such as impaired kidney function, certain medications, pregnancy, and rare genetic disorders. It is important to note that glycosuria alone does not necessarily indicate diabetes, but it may be a sign of an underlying medical condition that requires further evaluation by a healthcare professional.

Phlorhizin is not a medical condition or term, but rather a chemical compound. It is a glucoside that can be found in the bark of apple trees and other related plants. Phlorhizin has been studied in the field of medicine for its potential effects on various health conditions. Specifically, it has been shown to inhibit the enzyme called glucose transporter 2 (GLUT2), which is involved in the absorption of glucose in the body. As a result, phlorhizin has been investigated as a potential treatment for diabetes, as it may help regulate blood sugar levels. However, more research is needed to fully understand its effects and safety profile before it can be used as a medical treatment.

Gluconeogenesis is a metabolic pathway that occurs in the liver, kidneys, and to a lesser extent in the small intestine. It involves the synthesis of glucose from non-carbohydrate precursors such as lactate, pyruvate, glycerol, and certain amino acids. This process becomes particularly important during periods of fasting or starvation when glucose levels in the body begin to drop, and there is limited carbohydrate intake to replenish them.

Gluconeogenesis helps maintain blood glucose homeostasis by providing an alternative source of glucose for use by various tissues, especially the brain, which relies heavily on glucose as its primary energy source. It is a complex process that involves several enzymatic steps, many of which are regulated to ensure an adequate supply of glucose while preventing excessive production, which could lead to hyperglycemia.

Glucokinase is an enzyme that plays a crucial role in regulating glucose metabolism. It is primarily found in the liver, pancreas, and brain. In the pancreas, glucokinase helps to trigger the release of insulin in response to rising blood glucose levels. In the liver, it plays a key role in controlling glucose storage and production.

Glucokinase has a unique property among hexokinases (enzymes that phosphorylate six-carbon sugars) in that it is not inhibited by its product, glucose-6-phosphate. This allows it to continue functioning even when glucose levels are high, making it an important regulator of glucose metabolism.

Defects in the gene that codes for glucokinase can lead to several types of inherited diabetes and other metabolic disorders.

C-peptide is a byproduct that is produced when the hormone insulin is generated in the body. Insulin is a hormone that helps regulate blood sugar levels, and it is produced in the pancreas by specialized cells called beta cells. When these cells produce insulin, they also generate C-peptide as a part of the same process.

C-peptide is often used as a marker to measure the body's insulin production. By measuring C-peptide levels in the blood, healthcare providers can get an idea of how much insulin the body is producing on its own. This can be helpful in diagnosing and monitoring conditions such as diabetes, which is characterized by impaired insulin production or function.

It's worth noting that C-peptide is not typically used as a treatment for any medical conditions. Instead, it is primarily used as a diagnostic tool to help healthcare providers better understand their patients' health status and make informed treatment decisions.

Glucose intolerance is a condition in which the body has difficulty processing and using glucose, or blood sugar, effectively. This results in higher than normal levels of glucose in the blood after eating, particularly after meals that are high in carbohydrates. Glucose intolerance can be an early sign of developing diabetes, specifically type 2 diabetes, and it may also indicate other metabolic disorders such as prediabetes or insulin resistance.

In a healthy individual, the pancreas produces insulin to help regulate blood sugar levels by facilitating glucose uptake in muscles, fat tissue, and the liver. When someone has glucose intolerance, their body may not produce enough insulin, or their cells may have become less responsive to insulin (insulin resistance), leading to impaired glucose metabolism.

Glucose intolerance can be diagnosed through various tests, including the oral glucose tolerance test (OGTT) and hemoglobin A1c (HbA1c) test. Treatment for glucose intolerance often involves lifestyle modifications such as weight loss, increased physical activity, and a balanced diet with reduced sugar and refined carbohydrate intake. In some cases, medication may be prescribed to help manage blood sugar levels more effectively.

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC) is a serious complication of diabetes, specifically type 2, that occurs when blood glucose levels rise to extremely high levels, typically above 600 mg/dL. This condition is often accompanied by severe dehydration due to excessive urination and an inability to consume adequate fluids.

The term "hyperosmolar" refers to the high concentration of glucose in the blood, which increases the osmolality (or osmotic pressure) of the blood. This can lead to water moving out of cells and into the bloodstream to try to balance out the concentration, causing severe dehydration.

The term "nonketotic" means that there is no significant production of ketone bodies, which are produced when the body breaks down fat for energy in the absence of sufficient insulin. This differentiates HHNC from diabetic ketoacidosis (DKA), another serious complication of diabetes.

The "coma" part of the term refers to the fact that HHNC can cause altered mental status, ranging from confusion and disorientation to coma, due to the effects of dehydration and high blood glucose levels on the brain.

HHNC is a medical emergency that requires immediate treatment in a hospital setting. Treatment typically involves administering fluids to rehydrate the body, insulin to lower blood glucose levels, and addressing any other underlying conditions or complications. If left untreated, HHNC can be life-threatening.

Diabetic nephropathy is a kidney disease that occurs as a complication of diabetes. It is also known as diabetic kidney disease (DKD). This condition affects the ability of the kidneys to filter waste and excess fluids from the blood, leading to their accumulation in the body.

Diabetic nephropathy is caused by damage to the small blood vessels in the kidneys, which can occur over time due to high levels of glucose in the blood. This damage can lead to scarring and thickening of the kidney's filtering membranes, reducing their ability to function properly.

Symptoms of diabetic nephropathy may include proteinuria (the presence of protein in the urine), edema (swelling in the legs, ankles, or feet due to fluid retention), and hypertension (high blood pressure). Over time, if left untreated, diabetic nephropathy can progress to end-stage kidney disease, which requires dialysis or a kidney transplant.

Preventing or delaying the onset of diabetic nephropathy involves maintaining good control of blood sugar levels, keeping blood pressure under control, and making lifestyle changes such as quitting smoking, eating a healthy diet, and getting regular exercise. Regular monitoring of kidney function through urine tests and blood tests is also important for early detection and treatment of this condition.

Diabetic ketoacidosis (DKA) is a serious metabolic complication characterized by the triad of hyperglycemia, metabolic acidosis, and increased ketone bodies. It primarily occurs in individuals with diabetes mellitus type 1, but it can also be seen in some people with diabetes mellitus type 2, particularly during severe illness or surgery.

The condition arises when there is a significant lack of insulin in the body, which impairs the ability of cells to take up glucose for energy production. As a result, the body starts breaking down fatty acids to produce energy, leading to an increase in ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) in the bloodstream. This process is called ketosis.

In DKA, the excessive production of ketone bodies results in metabolic acidosis, which is characterized by a lower than normal pH level in the blood (< 7.35) and an elevated serum bicarbonate level (< 18 mEq/L). The hyperglycemia in DKA is due to both increased glucose production and decreased glucose utilization by cells, which can lead to severe dehydration and electrolyte imbalances.

Symptoms of diabetic ketoacidosis include excessive thirst, frequent urination, nausea, vomiting, abdominal pain, fatigue, fruity breath odor, and altered mental status. If left untreated, DKA can progress to coma and even lead to death. Treatment typically involves administering insulin, fluid replacement, and electrolyte management in a hospital setting.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

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.

Alloxan is a chemical compound that is primarily used in laboratory research. Its medical definition is:

A toxic, crystalline substance, C6H4O6, derived from uric acid, and used experimentally to produce diabetes in animals by destroying their insulin-producing cells (beta cells) in the pancreas. Alloxan monohydrate is a white crystalline powder that is soluble in water and alcohol. It is used as a reagent in analytical chemistry and in photography.

In scientific research, alloxan is often used to induce diabetes in laboratory animals (like rats and mice) in order to study the disease and potential treatments. The compound is toxic to the insulin-producing beta cells in the pancreas, leading to a decrease in insulin production and an increase in blood glucose levels, similar to what occurs in type 1 diabetes in humans. However, it's important to note that alloxan-induced diabetes does not perfectly mimic the human form of the disease, and results from such studies may not always translate directly to human treatments.

I'm sorry for any confusion, but "Rats, Zucker" is not a standard medical term or abbreviation in human medicine. It seems to be an incorrect combination of two terms from the field of laboratory animal science.

1. "Rats" are commonly used laboratory animals.
2. "Zucker" is a surname and also refers to a strain of laboratory rats, specifically the Zucker Diabetic Fatty (ZDF) rat, which is a model for studying type 2 diabetes mellitus.

If you have any questions related to human medicine or healthcare, I would be happy to help clarify those for you.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

'Pregnancy in Diabetics' refers to the condition where an individual with pre-existing diabetes mellitus becomes pregnant. This can be further categorized into two types:

1. Pre-gestational diabetes: This is when a woman is diagnosed with diabetes before she becomes pregnant. It includes both Type 1 and Type 2 diabetes. Proper control of blood sugar levels prior to conception and during pregnancy is crucial to reduce the risk of complications for both the mother and the baby.

2. Gestational diabetes: This is when a woman develops high blood sugar levels during pregnancy, typically in the second or third trimester. While it usually resolves after delivery, women with gestational diabetes have a higher risk of developing Type 2 diabetes later in life. Proper management of gestational diabetes is essential to ensure a healthy pregnancy and reduce the risk of complications for both the mother and the baby.

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.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

Obesity is a complex disease characterized by an excess accumulation of body fat to the extent that it negatively impacts health. It's typically defined using Body Mass Index (BMI), a measure calculated from a person's weight and height. A BMI of 30 or higher is indicative of obesity. However, it's important to note that while BMI can be a useful tool for identifying obesity in populations, it does not directly measure body fat and may not accurately reflect health status in individuals. Other factors such as waist circumference, blood pressure, cholesterol levels, and blood sugar levels should also be considered when assessing health risks associated with weight.

The pancreas is a glandular organ located in the abdomen, posterior to the stomach. It has both exocrine and endocrine functions. The exocrine portion of the pancreas consists of acinar cells that produce and secrete digestive enzymes into the duodenum via the pancreatic duct. These enzymes help in the breakdown of proteins, carbohydrates, and fats in food.

The endocrine portion of the pancreas consists of clusters of cells called islets of Langerhans, which include alpha, beta, delta, and F cells. These cells produce and secrete hormones directly into the bloodstream, including insulin, glucagon, somatostatin, and pancreatic polypeptide. Insulin and glucagon are critical regulators of blood sugar levels, with insulin promoting glucose uptake and storage in tissues and glucagon stimulating glycogenolysis and gluconeogenesis to raise blood glucose when it is low.

Nonketotic hyperglycinemia (NKH) is a rare inherited metabolic disorder characterized by an elevated level of the amino acid glycine in the body due to a deficiency of the enzyme needed to break it down, specifically the glycine cleavage system. This condition leads to developmental delays, seizures, and hypotonia (low muscle tone). The nonketotic part of the name refers to the fact that there is no production of ketones during periods of fasting or illness, which is unusual in disorders associated with elevated glycine levels.

NKH is typically caused by mutations in the GLDC or AMT gene and can be further classified into two types: type I (also known as the classic or severe form) and type II (also known as the attenuated or mild form). Type I NKH usually presents in early infancy with severe symptoms, including seizures, lethargy, and apnea, while type II NKH may present later in childhood with less severe symptoms.

Treatment for NKH is primarily supportive and includes anticonvulsant medications to manage seizures, as well as dietary management to limit glycine intake. In some cases, sodium benzoate or dextromethorphan may be used to reduce glycine levels in the body. However, there is no cure for NKH and prognosis varies depending on the severity of the condition.

Glucagon-like peptide 1 (GLP-1) is a hormone that is secreted by the intestines in response to food intake. It plays a crucial role in regulating blood sugar levels through several mechanisms, including stimulation of insulin secretion from the pancreas, inhibition of glucagon release, slowing gastric emptying, and promoting satiety. GLP-1 is an important target for the treatment of type 2 diabetes due to its insulin-secretory and glucose-lowering effects. In addition, GLP-1 receptor agonists are used in the management of obesity due to their ability to promote weight loss by reducing appetite and increasing feelings of fullness.

Chorea is a medical term that describes an involuntary movement disorder characterized by brief, irregular, and abrupt jerky movements. These movements often occur randomly and can affect any part of the body. Chorea can also cause difficulty with coordination and balance, and can sometimes be accompanied by muscle weakness or rigidity.

The term "chorea" comes from the Greek word "χορεία" (khoréia), which means "dance," reflecting the graceful, dance-like movements that are characteristic of this condition. Chorea can occur as a symptom of various underlying medical conditions, including neurological disorders such as Huntington's disease, Sydenham's chorea, and cerebral palsy, as well as metabolic disorders, infections, and certain medications.

Treatment for chorea depends on the underlying cause of the condition and may include medications to help control the involuntary movements, physical therapy to improve coordination and balance, and lifestyle modifications to reduce the risk of injury from falls or other accidents. In some cases, surgery may be recommended as a last resort for severe or refractory chorea.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Advanced Glycosylation End Products (AGEs) are formed through the non-enzymatic glycation and oxidative modification of proteins, lipids, and nucleic acids. This process occurs when a sugar molecule, such as glucose, binds to a protein or lipid without the regulation of an enzyme, leading to the formation of a Schiff base. This then rearranges to form a more stable ketoamine, known as an Amadori product. Over time, these Amadori products can undergo further reactions, including oxidation, fragmentation, and cross-linking, resulting in the formation of AGEs.

AGEs can alter the structure and function of proteins and lipids, leading to damage in tissues and organs. They have been implicated in the development and progression of several age-related diseases, including diabetes, atherosclerosis, kidney disease, and Alzheimer's disease. AGEs can also contribute to inflammation and oxidative stress, which can further exacerbate tissue damage.

In summary, Advanced Glycosylation End Products (AGEs) are the result of non-enzymatic glycation and oxidation of proteins, lipids, and nucleic acids, leading to structural and functional changes in tissues and organs, and contributing to the development and progression of several age-related diseases.

A prediabetic state, also known as impaired glucose tolerance or prediabetes, is a metabolic condition where blood sugar levels are higher than normal but not high enough to meet the diagnostic criteria for diabetes. It is often characterized by insulin resistance and beta-cell dysfunction, which can lead to an increased risk of developing type 2 diabetes, cardiovascular disease, and other complications if left untreated.

In the prediabetic state, fasting plasma glucose levels are between 100 and 125 mg/dL (5.6-6.9 mmol/L), or hemoglobin A1c (HbA1c) levels are between 5.7% and 6.4%. Lifestyle modifications, such as regular exercise, healthy eating habits, and weight loss, can help prevent or delay the progression of prediabetes to diabetes.

Diabetic retinopathy is a diabetes complication that affects the eyes. It's caused by damage to the blood vessels of the light-sensitive tissue at the back of the eye (retina).

At first, diabetic retinopathy may cause no symptoms or only mild vision problems. Eventually, it can cause blindness. The condition usually affects both eyes.

There are two main stages of diabetic retinopathy:

1. Early diabetic retinopathy. This is when the blood vessels in the eye start to leak fluid or bleed. You might not notice any changes in your vision at this stage, but it's still important to get treatment because it can prevent the condition from getting worse.
2. Advanced diabetic retinopathy. This is when new, abnormal blood vessels grow on the surface of the retina. These vessels can leak fluid and cause severe vision problems, including blindness.

Diabetic retinopathy can be treated with laser surgery, injections of medication into the eye, or a vitrectomy (a surgical procedure to remove the gel-like substance that fills the center of the eye). It's important to get regular eye exams to detect diabetic retinopathy early and get treatment before it causes serious vision problems.

Nonesterified fatty acids (NEFA), also known as free fatty acids (FFA), refer to fatty acid molecules that are not bound to glycerol in the form of triglycerides or other esters. In the bloodstream, NEFAs are transported while bound to albumin and can serve as a source of energy for peripheral tissues. Under normal physiological conditions, NEFA levels are tightly regulated by the body; however, elevated NEFA levels have been associated with various metabolic disorders such as insulin resistance, obesity, and type 2 diabetes.

Diabetic neuropathies refer to a group of nerve disorders that are caused by diabetes. High blood sugar levels can injure nerves throughout the body, but diabetic neuropathies most commonly affect the nerves in the legs and feet.

There are four main types of diabetic neuropathies:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy. It affects the nerves in the legs and feet, causing symptoms such as numbness, tingling, burning, or shooting pain.
2. Autonomic neuropathy: This type of neuropathy affects the autonomic nerves, which control involuntary functions such as heart rate, blood pressure, digestion, and bladder function. Symptoms may include dizziness, fainting, digestive problems, sexual dysfunction, and difficulty regulating body temperature.
3. Proximal neuropathy: Also known as diabetic amyotrophy, this type of neuropathy affects the nerves in the hips, thighs, or buttocks, causing weakness, pain, and difficulty walking.
4. Focal neuropathy: This type of neuropathy affects a single nerve or group of nerves, causing symptoms such as weakness, numbness, or pain in the affected area. Focal neuropathies can occur anywhere in the body, but they are most common in the head, torso, and legs.

The risk of developing diabetic neuropathies increases with the duration of diabetes and poor blood sugar control. Other factors that may contribute to the development of diabetic neuropathies include genetics, age, smoking, and alcohol consumption.

A critical illness is a serious condition that has the potential to cause long-term or permanent disability, or even death. It often requires intensive care and life support from medical professionals. Critical illnesses can include conditions such as:

1. Heart attack
2. Stroke
3. Organ failure (such as kidney, liver, or lung)
4. Severe infections (such as sepsis)
5. Coma or brain injury
6. Major trauma
7. Cancer that has spread to other parts of the body

These conditions can cause significant physical and emotional stress on patients and their families, and often require extensive medical treatment, rehabilitation, and long-term care. Critical illness insurance is a type of insurance policy that provides financial benefits to help cover the costs associated with treating these serious medical conditions.

Islets of Langerhans transplantation is a surgical procedure that involves the transplantation of isolated islets from a deceased donor's pancreas into another person with type 1 diabetes. The islets of Langerhans are clusters of cells within the pancreas that produce hormones, including insulin, which regulates blood sugar levels.

In type 1 diabetes, the body's immune system mistakenly attacks and destroys these insulin-producing cells, leading to high blood sugar levels. Islet transplantation aims to replace the damaged islets with healthy ones from a donor, allowing the recipient's body to produce and regulate its own insulin again.

The procedure involves extracting the islets from the donor pancreas and infusing them into the recipient's liver through a small incision in the abdomen. Once inside the liver, the islets can sense glucose levels in the bloodstream and release insulin as needed to maintain normal blood sugar levels.

Islet transplantation has shown promising results in improving blood sugar control and reducing the risk of severe hypoglycemia (low blood sugar) in people with type 1 diabetes. However, it requires long-term immunosuppressive therapy to prevent rejection of the transplanted islets, which can have side effects and increase the risk of infections.

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.

Fructosamine is a glycated protein that is formed when glucose binds to proteins in the bloodstream. It is used as an indicator of average blood glucose levels over the previous 2-3 weeks, and can be measured through a blood test. Fructosamine results are not affected by short-term changes in blood sugar levels or acute illnesses, making it useful for monitoring long-term glycemic control in people with diabetes.

The fructosamine test measures the level of glycated proteins in the blood, specifically those that have bound to serum albumin. The test results are reported as micromoles per liter (µmol/L) or millimoles per liter (mmol/L). Higher levels of fructosamine indicate poorer glucose control and an increased risk for diabetes complications, while lower levels suggest better glycemic control.

It's important to note that the fructosamine test is not a replacement for hemoglobin A1c (HbA1c) testing, which measures average blood glucose levels over the previous 2-3 months. Instead, it can be used as an additional tool in managing diabetes and assessing glycemic control.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

I cannot precisely define "obese mice" from a medical perspective because "obesity" is typically defined for humans and companion animals based on body weight relative to body size. However, I can provide you with relevant information regarding obese mice in a research or laboratory context.

Obesity in mice is often induced by providing them with a high-fat diet (HFD) to promote excessive weight gain and metabolic dysfunction. This allows researchers to study the effects of obesity on various health parameters, such as insulin resistance, inflammation, and cardiovascular function.

In laboratory settings, mice are often considered obese if their body weight is 10-20% higher than the average for their strain, age, and sex. Researchers also use body mass index (BMI) or body fat percentage to determine obesity in mice. For example:

* Body Mass Index (BMI): Mice with a BMI greater than 0.69 g/cm² are considered obese. To calculate BMI, divide the body weight in grams by the square of the nose-to-anus length in centimeters.
* Body Fat Percentage: Obesity can also be determined based on body fat percentage using non-invasive methods like magnetic resonance imaging (MRI) or computed tomography (CT) scans. Mice with more than 45% body fat are generally considered obese.

It is important to note that these thresholds may vary depending on the mouse strain, age, and sex. Researchers should consult relevant literature for their specific experimental setup when defining obesity in mice.

Reference values, also known as reference ranges or reference intervals, are the set of values that are considered normal or typical for a particular population or group of people. These values are often used in laboratory tests to help interpret test results and determine whether a patient's value falls within the expected range.

The process of establishing reference values typically involves measuring a particular biomarker or parameter in a large, healthy population and then calculating the mean and standard deviation of the measurements. Based on these statistics, a range is established that includes a certain percentage of the population (often 95%) and excludes extreme outliers.

It's important to note that reference values can vary depending on factors such as age, sex, race, and other demographic characteristics. Therefore, it's essential to use reference values that are specific to the relevant population when interpreting laboratory test results. Additionally, reference values may change over time due to advances in measurement technology or changes in the population being studied.

Glucose Transporter Type 2 (GLUT2) is a protein responsible for the facilitated diffusion of glucose across the cell membrane. It is a member of the solute carrier family 2 (SLC2), also known as the facilitative glucose transporter family. GLUT2 is primarily expressed in the liver, kidney, and intestines, where it plays a crucial role in regulating glucose homeostasis.

In the pancreas, GLUT2 is found in the beta cells of the islets of Langerhans, where it facilitates the uptake of glucose from the bloodstream into the cells. Once inside the cell, glucose is metabolized, leading to an increase in ATP levels and the closure of ATP-sensitive potassium channels. This results in the depolarization of the cell membrane and the subsequent opening of voltage-gated calcium channels, allowing for the release of insulin from secretory vesicles into the bloodstream.

In the intestines, GLUT2 is expressed in the enterocytes of the small intestine, where it facilitates the absorption of glucose and other monosaccharides from the lumen into the bloodstream. In the kidneys, GLUT2 is found in the proximal tubules, where it plays a role in reabsorbing glucose from the filtrate back into the bloodstream.

Mutations in the gene that encodes GLUT2 (SLC2A2) can lead to several genetic disorders, including Fanconi-Bickel syndrome, which is characterized by impaired glucose and galactose absorption in the intestines, hepatic glycogen accumulation, and renal tubular dysfunction.

Acarbose is a medication that belongs to a class of drugs called alpha-glucosidase inhibitors. It is used in the management of type 2 diabetes mellitus. Acarbose works by slowing down the digestion of carbohydrates in the small intestine, which helps to prevent spikes in blood sugar levels after meals.

By blocking the enzyme alpha-glucosidase, acarbose prevents the breakdown of complex carbohydrates into simple sugars, such as glucose, in the small intestine. This results in a slower and more gradual absorption of glucose into the bloodstream, which helps to prevent postprandial hyperglycemia (high blood sugar levels after meals).

Acarbose is typically taken orally three times a day, before meals containing carbohydrates. Common side effects include gastrointestinal symptoms such as bloating, flatulence, and diarrhea. It is important to note that acarbose should be used in conjunction with a healthy diet and regular exercise to effectively manage blood sugar levels in individuals with type 2 diabetes.

Glycogenolysis is the biochemical process by which glycogen, a polymer of glucose, is broken down into its constituent glucose molecules. This process occurs primarily in the liver and muscles and is critical for maintaining normal blood glucose levels between meals and during periods of increased physical activity.

Glycogenolysis is initiated by the enzyme glycogen phosphorylase, which cleaves off individual glucose molecules from the end of a glycogen branch, resulting in the formation of glucose-1-phosphate. This compound is then converted to glucose-6-phosphate by the enzyme phosphoglucomutase.

Glucose-6-phosphate can be further metabolized through several pathways, including glycolysis or the pentose phosphate pathway, depending on the energy needs of the cell. In the liver, glucose-6-phosphatase can remove the phosphate group from glucose-6-phosphate to produce free glucose, which is released into the bloodstream and transported to other tissues for use as an energy source.

Overall, glycogenolysis plays a crucial role in maintaining normal blood glucose levels and providing energy to cells during periods of increased demand.

"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.

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.

Intravenous (IV) infusion is a medical procedure in which liquids, such as medications, nutrients, or fluids, are delivered directly into a patient's vein through a needle or a catheter. This route of administration allows for rapid absorption and distribution of the infused substance throughout the body. IV infusions can be used for various purposes, including resuscitation, hydration, nutrition support, medication delivery, and blood product transfusion. The rate and volume of the infusion are carefully controlled to ensure patient safety and efficacy of treatment.

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

Hexosamines are amino sugars that are formed by the substitution of an amino group (-NH2) for a hydroxyl group (-OH) in a hexose sugar. The most common hexosamine is N-acetylglucosamine (GlcNAc), which is derived from glucose. Other hexosamines include galactosamine, mannosamine, and fucosamine.

Hexosamines play important roles in various biological processes, including the formation of glycosaminoglycans, proteoglycans, and glycoproteins. These molecules are involved in many cellular functions, such as cell signaling, cell adhesion, and protein folding. Abnormalities in hexosamine metabolism have been implicated in several diseases, including diabetes, cancer, and neurodegenerative disorders.

Glycogen is a complex carbohydrate that serves as the primary form of energy storage in animals, fungi, and bacteria. It is a polysaccharide consisting of long, branched chains of glucose molecules linked together by glycosidic bonds. Glycogen is stored primarily in the liver and muscles, where it can be quickly broken down to release glucose into the bloodstream during periods of fasting or increased metabolic demand.

In the liver, glycogen plays a crucial role in maintaining blood glucose levels by releasing glucose when needed, such as between meals or during exercise. In muscles, glycogen serves as an immediate energy source for muscle contractions during intense physical activity. The ability to store and mobilize glycogen is essential for the proper functioning of various physiological processes, including athletic performance, glucose homeostasis, and overall metabolic health.

Gestational diabetes is a type of diabetes that occurs during pregnancy. It is characterized by an increase in blood sugar levels that begins or is first recognized during pregnancy. The condition usually develops around the 24th week of gestation and is caused by the body's inability to produce enough insulin to meet the increased demands of pregnancy.

Gestational diabetes typically resolves after delivery, but women who have had gestational diabetes are at an increased risk of developing type 2 diabetes later in life. It is important for women with gestational diabetes to manage their blood sugar levels during pregnancy to reduce the risk of complications for both the mother and the baby.

Management of gestational diabetes may include lifestyle modifications such as dietary changes and exercise, as well as monitoring blood sugar levels and potentially using insulin or other medications to control blood sugar levels. Regular prenatal care is essential for women with gestational diabetes to ensure that their blood sugar levels are properly managed and to monitor the growth and development of the fetus.

Glucose-6-phosphatase is an enzyme that plays a crucial role in the regulation of glucose metabolism. It is primarily located in the endoplasmic reticulum of cells in liver, kidney, and intestinal mucosa. The main function of this enzyme is to remove the phosphate group from glucose-6-phosphate (G6P), converting it into free glucose, which can then be released into the bloodstream and used as a source of energy by cells throughout the body.

The reaction catalyzed by glucose-6-phosphatase is as follows:

Glucose-6-phosphate + H2O → Glucose + Pi (inorganic phosphate)

This enzyme is essential for maintaining normal blood glucose levels, particularly during periods of fasting or starvation. In these situations, the body needs to break down stored glycogen in the liver and convert it into glucose to supply energy to the brain and other vital organs. Glucose-6-phosphatase is a key enzyme in this process, allowing for the release of free glucose into the bloodstream.

Deficiencies or mutations in the gene encoding glucose-6-phosphatase can lead to several metabolic disorders, such as glycogen storage disease type I (von Gierke's disease) and other related conditions. These disorders are characterized by an accumulation of glycogen and/or fat in various organs, leading to impaired glucose metabolism, growth retardation, and increased risk of infection and liver dysfunction.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Liver glycogen is the reserve form of glucose stored in hepatocytes (liver cells) for the maintenance of normal blood sugar levels. It is a polysaccharide, a complex carbohydrate, that is broken down into glucose molecules when blood glucose levels are low. This process helps to maintain the body's energy needs between meals and during periods of fasting or exercise. The amount of glycogen stored in the liver can vary depending on factors such as meal consumption, activity level, and insulin regulation.

Homeostasis is a fundamental concept in the field of medicine and physiology, referring to the body's ability to maintain a stable internal environment, despite changes in external conditions. It is the process by which biological systems regulate their internal environment to remain in a state of dynamic equilibrium. This is achieved through various feedback mechanisms that involve sensors, control centers, and effectors, working together to detect, interpret, and respond to disturbances in the system.

For example, the body maintains homeostasis through mechanisms such as temperature regulation (through sweating or shivering), fluid balance (through kidney function and thirst), and blood glucose levels (through insulin and glucagon secretion). When homeostasis is disrupted, it can lead to disease or dysfunction in the body.

In summary, homeostasis is the maintenance of a stable internal environment within biological systems, through various regulatory mechanisms that respond to changes in external conditions.

Deoxyglucose is a glucose molecule that has had one oxygen atom removed, resulting in the absence of a hydroxyl group (-OH) at the 2' position of the carbon chain. It is used in research and medical settings as a metabolic tracer to study glucose uptake and metabolism in cells and organisms.

Deoxyglucose can be taken up by cells through glucose transporters, but it cannot be further metabolized by glycolysis or other glucose-utilizing pathways. This leads to the accumulation of deoxyglucose within the cell, which can interfere with normal cellular processes and cause toxicity in high concentrations.

In medical research, deoxyglucose is sometimes labeled with radioactive isotopes such as carbon-14 or fluorine-18 to create radiolabeled deoxyglucose (FDG), which can be used in positron emission tomography (PET) scans to visualize and measure glucose uptake in tissues. This technique is commonly used in cancer imaging, as tumors often have increased glucose metabolism compared to normal tissue.

Aldehyde reductase is an enzyme that belongs to the family of alcohol dehydrogenases. Its primary function is to catalyze the reduction of a wide variety of aldehydes into their corresponding alcohols, using NADPH as a cofactor. This enzyme plays a crucial role in the detoxification of aldehydes generated from various metabolic processes, such as lipid peroxidation and alcohol metabolism. It is widely distributed in different tissues, including the liver, kidney, and brain. In addition to its detoxifying function, aldehyde reductase has been implicated in several physiological and pathophysiological processes, such as neuroprotection, cancer, and diabetes.

Metformin is a type of biguanide antihyperglycemic agent used primarily in the treatment of type 2 diabetes mellitus. It works by decreasing glucose production in the liver, reducing glucose absorption in the gut, and increasing insulin sensitivity in muscle and fat tissue. By lowering both basal and postprandial plasma glucose levels, metformin helps to control blood sugar levels and improve glycemic control. It is also used off-label for various other indications such as polycystic ovary syndrome (PCOS) and gestational diabetes. Common side effects include diarrhea, nausea, vomiting, and abdominal discomfort. Lactic acidosis is a rare but serious side effect that requires immediate medical attention.

A diabetic coma is a serious and life-threatening condition that occurs when an individual with diabetes experiences severely high or low blood sugar levels, leading to unconsciousness. It is a medical emergency that requires immediate attention.

In the case of hyperglycemia (high blood sugar), the body produces excess amounts of urine to try to eliminate the glucose, leading to dehydration and a lack of essential nutrients in the body. This can result in a buildup of toxic byproducts called ketones, which can cause a condition known as diabetic ketoacidosis (DKA). DKA can lead to a diabetic coma if left untreated.

On the other hand, hypoglycemia (low blood sugar) can also cause a diabetic coma. This occurs when the brain is not receiving enough glucose to function properly, leading to confusion, seizures, and eventually unconsciousness.

If you suspect someone is experiencing a diabetic coma, it is important to seek emergency medical attention immediately. While waiting for help to arrive, try to administer glucose or sugar to the individual if they are conscious and able to swallow. If they are unconscious, do not give them anything to eat or drink, as this could cause choking or further complications.

Proinsulin is the precursor protein to insulin, produced in the beta cells of the pancreas. It has a molecular weight of around 9,000 daltons and is composed of three distinct regions: the A-chain, the B-chain, and the C-peptide. The A-chain and B-chain are linked together by disulfide bonds and will eventually become the insulin molecule after a series of enzymatic cleavages. The C-peptide is removed during this process and is released into the bloodstream in equimolar amounts to insulin. Proinsulin levels can be measured in the blood and are sometimes used as a marker for beta cell function in certain clinical settings, such as diagnosing or monitoring insulinoma (a tumor of the pancreas that produces insulin) or assessing the risk of diabetes-related complications.

Sodium-Glucose Transporter 2 (SGLT2) is a medically recognized term referring to a specific protein that plays a crucial role in the reabsorption of glucose in the kidneys. It is a type of membrane transport protein located in the proximal convoluted tubule of the nephron, where it actively transports glucose and sodium ions from the urine back into the bloodstream.

In healthy individuals, SGLT2 is responsible for reabsorbing about 90% of the filtered glucose, maintaining normal blood glucose levels. However, in certain medical conditions like diabetes, the amount of glucose in the blood can be significantly higher than normal. As a result, SGLT2 inhibitors have been developed as a class of medications to block this transporter's function, thereby increasing glucose excretion through urine and lowering blood glucose levels.

SGLT2 inhibitors are often prescribed in combination with other diabetes medications to help manage type 2 diabetes more effectively. Common SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.

Glucagon-secreting cells, also known as alpha (α) cells, are a type of cell located in the pancreatic islets of Langerhans. These cells are responsible for producing and secreting the hormone glucagon, which plays a crucial role in regulating blood glucose levels.

Glucagon works in opposition to insulin, another hormone produced by different cells in the pancreas called beta (β) cells. When blood glucose levels are low, such as during fasting or exercise, glucagon is released into the bloodstream and travels to the liver, where it stimulates the breakdown of glycogen (stored glucose) into glucose, which is then released into the bloodstream to raise blood glucose levels.

Abnormalities in glucagon-secreting cells can contribute to various endocrine disorders, such as diabetes and hypoglycemia.

Somatostatin is a hormone that inhibits the release of several hormones and also has a role in slowing down digestion. It is produced by the body in various parts of the body, including the hypothalamus (a part of the brain), the pancreas, and the gastrointestinal tract.

Somatostatin exists in two forms: somatostatin-14 and somatostatin-28, which differ in their length. Somatostatin-14 is the predominant form found in the brain, while somatostatin-28 is the major form found in the gastrointestinal tract.

Somatostatin has a wide range of effects on various physiological processes, including:

* Inhibiting the release of several hormones such as growth hormone, insulin, glucagon, and gastrin
* Slowing down digestion by inhibiting the release of digestive enzymes from the pancreas and reducing blood flow to the gastrointestinal tract
* Regulating neurotransmission in the brain

Somatostatin is used clinically as a diagnostic tool for detecting certain types of tumors that overproduce growth hormone or other hormones, and it is also used as a treatment for some conditions such as acromegaly (a condition characterized by excessive growth hormone production) and gastrointestinal disorders.

An Insulin Infusion System, also known as an insulin pump, is a medical device designed to deliver insulin in a continuous and controlled manner. It consists of a small computerized device that is worn outside the body, connected to a thin tube called a cannula which is inserted under the skin using a needle. The cannula is typically changed every 2-3 days.

The system allows for the programming of basal rates (background insulin), as well as bolus doses (additional insulin given at mealtimes or to correct high blood glucose levels). The user has the ability to customize these settings based on their individual needs, which can be particularly useful for people with type 1 diabetes who require multiple daily injections of insulin.

Insulin infusion systems are designed to mimic the normal physiological release of insulin from the pancreas more closely than traditional injection methods, and they have been shown to improve glycemic control and quality of life for some people with diabetes. However, they also require a significant amount of user education and training to ensure safe and effective use.

Metabolic syndrome, also known as Syndrome X, is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes. It is not a single disease but a group of risk factors that often co-occur. According to the American Heart Association and the National Heart, Lung, and Blood Institute, a person has metabolic syndrome if they have any three of the following five conditions:

1. Abdominal obesity (waist circumference of 40 inches or more in men, and 35 inches or more in women)
2. Triglyceride level of 150 milligrams per deciliter of blood (mg/dL) or greater
3. HDL cholesterol level of less than 40 mg/dL in men or less than 50 mg/dL in women
4. Systolic blood pressure of 130 millimeters of mercury (mmHg) or greater, or diastolic blood pressure of 85 mmHg or greater
5. Fasting glucose level of 100 mg/dL or greater

Metabolic syndrome is thought to be caused by a combination of genetic and lifestyle factors, such as physical inactivity and a diet high in refined carbohydrates and unhealthy fats. Treatment typically involves making lifestyle changes, such as eating a healthy diet, getting regular exercise, and losing weight if necessary. In some cases, medication may also be needed to manage individual components of the syndrome, such as high blood pressure or high cholesterol.

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.

Sorbitol is a type of sugar alcohol used as a sweetener in food and drinks, with about half the calories of table sugar. In a medical context, sorbitol is often used as a laxative to treat constipation, or as a sugar substitute for people with diabetes. It's also used as a bulk sweetener and humectant (a substance that helps retain moisture) in various pharmaceutical and cosmetic products.

When consumed in large amounts, sorbitol can have a laxative effect because it's not fully absorbed by the body and draws water into the intestines, which can lead to diarrhea. It's important for people with certain digestive disorders, such as irritable bowel syndrome or fructose intolerance, to avoid sorbitol and other sugar alcohols, as they can cause gastrointestinal symptoms like bloating, gas, and diarrhea.

Blood glucose self-monitoring is the regular measurement of blood glucose levels performed by individuals with diabetes to manage their condition. This process involves using a portable device, such as a glucometer or continuous glucose monitor (CGM), to measure the amount of glucose present in a small sample of blood, usually obtained through a fingerstick.

The primary purpose of self-monitoring is to help individuals with diabetes understand how various factors, such as food intake, physical activity, medication, and stress, affect their blood glucose levels. By tracking these patterns, they can make informed decisions about adjusting their diet, exercise, or medication regimens to maintain optimal glycemic control and reduce the risk of long-term complications associated with diabetes.

Self-monitoring is an essential component of diabetes self-management and education, enabling individuals to take an active role in their healthcare. Regular monitoring also allows healthcare professionals to assess a patient's adherence to their treatment plan and make necessary adjustments based on the data collected.

Glucagon receptors are a type of G protein-coupled receptor found on the surface of cells in the body, particularly in the liver, fat, and muscle tissues. These receptors bind to the hormone glucagon, which is produced and released by the alpha cells of the pancreas in response to low blood sugar levels (hypoglycemia).

When glucagon binds to its receptor, it triggers a series of intracellular signaling events that lead to the breakdown of glycogen (a stored form of glucose) in the liver and the release of glucose into the bloodstream. This helps to raise blood sugar levels back to normal.

Glucagon receptors also play a role in regulating fat metabolism, as activation of these receptors in adipose tissue can stimulate the breakdown of triglycerides (a type of fat) into free fatty acids and glycerol, which can then be used as energy sources.

Abnormalities in glucagon receptor function or expression have been implicated in various metabolic disorders, including diabetes and obesity.

Lactates, also known as lactic acid, are compounds that are produced by muscles during intense exercise or other conditions of low oxygen supply. They are formed from the breakdown of glucose in the absence of adequate oxygen to complete the full process of cellular respiration. This results in the production of lactate and a hydrogen ion, which can lead to a decrease in pH and muscle fatigue.

In a medical context, lactates may be measured in the blood as an indicator of tissue oxygenation and metabolic status. Elevated levels of lactate in the blood, known as lactic acidosis, can indicate poor tissue perfusion or hypoxia, and may be seen in conditions such as sepsis, cardiac arrest, and severe shock. It is important to note that lactates are not the primary cause of acidemia (low pH) in lactic acidosis, but rather a marker of the underlying process.

Chronic hyperglycemia can be measured via the HbA1c test. The definition of acute hyperglycemia varies by study, with mmol/L ... Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with ... In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in ... Also, patients with immune-mediated diabetes, can change from modest fasting hyperglycemia to severe hyperglycemia and even ...
... (also called stress diabetes or diabetes of injury) is a medical term referring to transient elevation of ... Diagnosing patient can be complex, as there are no guidelines that specifically define stress hyperglycemia. One of the most ... Dungan KM, Braithwaite SS, Preiser JC (July 2011). "Stress hyperglycaemia". The Lancet. 373 (9677): 1798-1807. doi:10.1016/ ... "Stress hyperglycaemia in critically ill patients and the subsequent risk of diabetes: a systematic review and meta-analysis". ...
If an IV infusion of 10% dextrose in water is initiated then the nurse must monitor for: •Circulatory overload •Hyperglycemia • ...
The examples of short- term effects created by glucocorticoids are hyperglycemia, oscillation in blood pressure, psychiatric ... Kwon, Soonho; Hermayer, Kathie L.; Hermayer, Kathie (2013-04-01). "Glucocorticoid-Induced Hyperglycemia". The American Journal ...
... indicating severe hyperglycemia. When Barnbaum's physician assistant saw the test results, he immediately called police, who ...
Hyperglycemia, or high blood sugar, can increase frequency of seizure. The probable mechanism is that elevated extracellular ... Epilepsy Foundation Stafstrom, Carl E. (July 2003). "Hyperglycemia Lowers Seizure Threshold". Epilepsy Currents. 3 (4): 148-149 ...
Somogyi, M; Kirstein, M (1938). "Insulin as a cause of extreme hyperglycemia and instability". Weekly Bulletin of the St Louis ... The Chronic Somogyi rebound, a form of post-hypoglycemic hyperglycemia that Somogyi theorized could occur as a defensive ... As of 2011-05-28, the electronic text is not open access). "Somogyi Phenomenon - Rebound Hyperglycemia". Diabetes.co.uk. 15 ...
Hiebert Linda M.; Han Juying & Mandal Anil Kumar (2014). "Glycosaminoglycans, Hyperglycemia, and Disease". Antioxidants & Redox ...
Johnson, SF; Loge, RV (Mar 1988). "Palinopsia due to nonketotic hyperglycemia". The Western Journal of Medicine. 148 (3): 331-2 ... Causes of seizures that are reported to cause palinopsia include metabolic disturbances (hyperglycemia, carnitine deficiency), ...
"Hyperglycemia associated with olanzapine treatment". Indian J Psychiatry. 53 (2): 176-7. doi:10.4103/0019-5545.82562. PMC ...
Saydah SH, Miret M, Sung J, Varas C, Gause D, Brancati FL (August 2001). "Postchallenge hyperglycemia and mortality in a ... Stahl SJ (2006-01-01). "Chapter 58 - Hyperglycemia in Reptiles". In Mader DR (ed.). Reptile Medicine and Surgery (Second ed.). ... Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: Report of a WHO/IDF consultation (PDF). Geneva: ... Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation (PDF). World ...
Hyperglycemia may be present, as glucose consumption by cells and insulin secretion both decrease, and tissue sensitivity to ... Marx 2010 p.1869 Altus P, Hickman JW (May 1981). "Accidental hypothermia: hypoglycemia or hyperglycemia". Western Journal of ...
"Hyperglycemia in diabetes - Symptoms and causes". Mayo Clinic. Retrieved 2022-03-22. Wang, Jigang; Xu, Chengchao; Wong, Yin ... They discovered that "insulin-induced hypoglycemia was preceded by a transient, rather mild hyperglycemia..." Murlin is ...
Hyperglycemia can lead to neutrophil dysfunction. Dysfunction in the neutrophil biochemical pathway myeloperoxidase as well as ... Xiu F, Stanojcic M, Diao L, Jeschke MG (8 May 2014). "Stress hyperglycemia, insulin treatment, and innate immune cells". ... reduced degranulation are associated with hyperglycemia. The Absolute neutrophil count (ANC) is also used in diagnosis and ...
Hyperglycemia Hypoglycemia Khatib, Oussama MN (2006). Guidelines for the prevention, management and care of diabetes mellitus. ... Glucose tests can reveal temporary/long-term hyperglycemia or hypoglycemia. These conditions may not have obvious symptoms and ...
These effects cause maintenance of hyperglycemia. Because sodium is absorbed at the same time as glucose via SGLT-2, the ...
Hyperglycemia is common at the start of therapy, but can be treated with insulin added to the TPN solution. Hypoglycaemia is ... This can be related to hyperglycemia. Pregnancy can cause major complications when trying to properly dose the nutrient mixture ... Other than those listed below, common complications of TPN include hypophosphatemia, hypokalemia, hyperglycemia, hypercapnia, ... effectiveness in prevention of hyperglycemia and infectious complications-a randomized clinical trial". Critical Care Medicine ...
Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is ...
June 2012). "Management of hyperglycemia in type 2 diabetes: a patient-centered approach: position statement of the American ... Suchard JR, Grotsky TA (August 2008). "Fatal metformin overdose presenting with progressive hyperglycemia". The Western Journal ... "Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of ... hypoglycemia or hyperglycemia. Treatment of metformin overdose is generally supportive, as no specific antidote is known. ...
Kylin E (1923). "[Studies of the hypertension-hyperglycemia-hyperuricemia syndrome]". Zentralbl Inn Med (in German). 44: 105- ... or use of medication for hyperglycemia The Cardiometabolic index (CMI) is a tool used to calculate risk of type 2 diabetes, non ...
Hyperglycemia is also a common side effect.[citation needed] The tendency, as for all loop diuretics, to cause low serum ...
... hyperglycemia. Risk of progression; direct evidence by periapical radiographs of CAL loss, or indirect (bone/age ratio). "What ...
Hyperglycemia (diabetic coma) and Hypoglycemia (insulin shock). Hypothermia, or Exposure, occurs when a person's core body ...
Energetics of Cellular Respiration (Glucose Metabolism). Lebovitz, Harold E. (2016). "Hyperglycemia Secondary to Nondiabetic ...
One simple way to determine if nocturnal hypoglycemia may be causing morning hyperglycemia is to have the patient have a high ... Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to ... Michael Somogyi (www.whonamedit.com) Somogyi, M; Kirstein, M (1938). "Insulin as a cause of extreme hyperglycemia and ... Occasionally, insufficient insulin can result in hyperglycemia. The appropriate response is to take a correction dose of ...
March 1993). "Familial hyperglycemia due to mutations in glucokinase. Definition of a subtype of diabetes mellitus". The New ...
The resultant hyperglycemia promotes further insulin release. As glucose concentration eventually falls, insulin secretion also ...
"Hyperglycaemia and pulmonary infection". Proceedings of the Nutrition Society. 65 (3): 227-235. doi:10.1079/PNS2006499. ISSN ...
However, the low insulin levels seen in diabetes result in hyperglycemia, where glucose levels in the blood rise and glucose is ... Hepatocytes further contribute to this hyperglycemia through gluconeogenesis. Glycolysis in hepatocytes controls hepatic ... thus preventing hyperglycemia by storing the excess glucose as fat or glycogen, depending on the tissue type). The liver is ... hyperglycemia results. Glycolytic mutations are generally rare due to importance of the metabolic pathway; the majority of ...
Persistent hyperglycemia and glucosuria are very commonly seen. Hyperlipidemia may be present, especially in ponies. Other ... Attitude, activity levels, hyperglycemia, and increased drinking and urination are usually improved within 30 days of ...

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