Disorders in the processing of iron in the body: its absorption, transport, storage, and utilization. (From Mosby's Medical, Nursing, & Allied Health Dictionary, 4th ed)
Pathological conditions resulting from abnormal anabolism or catabolism of lipids in the body.
Disorders in the processing of calcium in the body: its absorption, transport, storage, and utilization.
A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN.
Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)
Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.
Organic chemicals that form two or more coordination links with an iron ion. Once coordination has occurred, the complex formed is called a chelate. The iron-binding porphyrin group of hemoglobin is an example of a metal chelate found in biological systems.
Forms of hepcidin, a cationic amphipathic peptide synthesized in the liver as a prepropeptide which is first processed into prohepcidin and then into the biologically active hepcidin forms, including in human the 20-, 22-, and 25-amino acid residue peptide forms. Hepcidin acts as a homeostatic regulators of iron metabolism and also possesses antimicrobial activity.
Iron-containing proteins that are widely distributed in animals, plants, and microorganisms. Their major function is to store IRON in a nontoxic bioavailable form. Each ferritin molecule consists of ferric iron in a hollow protein shell (APOFERRITINS) made of 24 subunits of various sequences depending on the species and tissue types.
An excessive accumulation of iron in the body due to a greater than normal absorption of iron from the gastrointestinal tract or from parenteral injection. This may arise from idiopathic hemochromatosis, excessive iron intake, chronic alcoholism, certain types of refractory anemia, or transfusional hemosiderosis. (From Churchill's Illustrated Medical Dictionary, 1989)
A multifunctional iron-sulfur protein that is both an iron regulatory protein and cytoplasmic form of aconitate hydratase. It binds to iron regulatory elements found on mRNAs involved in iron metabolism and regulates their translation. Its RNA binding ability and its aconitate hydrolase activity are dependent upon availability of IRON.
A multifunctional iron-sulfur protein that is both an iron regulatory protein and cytoplasmic form of aconitate hydratase. It binds to iron regulatory elements found on mRNAs involved in iron metabolism and regulates their translation. Its rate of degradation is increased in the presence of IRON.
Proteins that regulate cellular and organismal iron homeostasis. They play an important biological role by maintaining iron levels that are adequate for metabolic need, but below the toxicity threshold.
A disorder of iron metabolism characterized by a triad of HEMOSIDEROSIS; LIVER CIRRHOSIS; and DIABETES MELLITUS. It is caused by massive iron deposits in parenchymal cells that may develop after a prolonged increase of iron absorption. (Jablonski's Dictionary of Syndromes & Eponymic Diseases, 2d ed)
Membrane glycoproteins found in high concentrations on iron-utilizing cells. They specifically bind iron-bearing transferrin, are endocytosed with its ligand and then returned to the cell surface where transferrin without its iron is released.
An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.
Small cationic peptides that are an important component, in most species, of early innate and induced defenses against invading microbes. In animals they are found on mucosal surfaces, within phagocytic granules, and on the surface of the body. They are also found in insects and plants. Among others, this group includes the DEFENSINS, protegrins, tachyplesins, and thionins. They displace DIVALENT CATIONS from phosphate groups of MEMBRANE LIPIDS leading to disruption of the membrane.
Iron or iron compounds used in foods or as food. Dietary iron is important in oxygen transport and the synthesis of the iron-porphyrin proteins hemoglobin, myoglobin, cytochromes, and cytochrome oxidase. Insufficient amounts of dietary iron can lead to iron-deficiency anemia.
Stable iron atoms that have the same atomic number as the element iron, but differ in atomic weight. Fe-54, 57, and 58 are stable iron isotopes.
Anemia characterized by decreased or absent iron stores, low serum iron concentration, low transferrin saturation, and low hemoglobin concentration or hematocrit value. The erythrocytes are hypochromic and microcytic and the iron binding capacity is increased.
Membrane proteins whose primary function is to facilitate the transport of positively charged molecules (cations) across a biological membrane.
Unstable isotopes of iron that decay or disintegrate emitting radiation. Fe atoms with atomic weights 52, 53, 55, and 59-61 are radioactive iron isotopes.
Proteins that specifically bind to IRON.
The protein components of ferritins. Apoferritins are shell-like structures containing nanocavities and ferroxidase activities. Apoferritin shells are composed of 24 subunits, heteropolymers in vertebrates and homopolymers in bacteria. In vertebrates, there are two types of subunits, light chain and heavy chain. The heavy chain contains the ferroxidase activity.
Ceruloplasmin is a blue copper-containing protein primarily synthesized in the liver, functioning as a ferroxidase enzyme involved in iron homeostasis and contributing to copper transportation in the body.
A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence.
Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.
An enzyme that catalyzes the reversible hydration of cis-aconitate to yield citrate or isocitrate. It is one of the citric acid cycle enzymes. EC 4.2.1.3.
Inorganic or organic compounds containing trivalent iron.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
A group of proteins possessing only the iron-sulfur complex as the prosthetic group. These proteins participate in all major pathways of electron transport: photosynthesis, respiration, hydroxylation and bacterial hydrogen and nitrogen fixation.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. The individual cells contain less hemoglobin than they could have under optimal conditions. Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections or other diseases, therapeutic drugs, lead poisoning, and other conditions. (Stedman, 25th ed; from Miale, Laboratory Medicine: Hematology, 6th ed, p393)
Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function.
An enzyme that utilizes NADH or NADPH to reduce FLAVINS. It is involved in a number of biological processes that require reduced flavin for their functions such as bacterial bioluminescence. Formerly listed as EC 1.6.8.1 and EC 1.5.1.29.
Low-molecular-weight compounds produced by microorganisms that aid in the transport and sequestration of ferric iron. (The Encyclopedia of Molecular Biology, 1994)
Persistent and disabling ANXIETY.
Those disorders that have a disturbance in mood as their predominant feature.
Inorganic or organic compounds that contain divalent iron.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
Inborn errors of metal metabolism refer to genetic disorders resulting from mutations in genes encoding proteins involved in the transportation, storage, or utilization of essential metals, leading to imbalances that can cause toxicity or deficiency and subsequent impairment of normal physiological processes.
The production of red blood cells (ERYTHROCYTES). In humans, erythrocytes are produced by the YOLK SAC in the first trimester; by the liver in the second trimester; by the BONE MARROW in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction.
Organic and inorganic compounds that contain iron as an integral part of the molecule.
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.
The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins.
Categorical classification of MENTAL DISORDERS based on criteria sets with defining features. It is produced by the American Psychiatric Association. (DSM-IV, page xxii)
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

Clinical severity and thermodynamic effects of iron-responsive element mutations in hereditary hyperferritinemia-cataract syndrome. (1/114)

Hereditary hyperferritinemia-cataract syndrome (HHCS) is a novel genetic disorder characterized by elevated serum ferritin and early onset cataract formation. The excessive ferritin production in HHCS patients arises from aberrant regulation of L-ferritin translation caused by mutations within the iron-responsive element (IRE) of the L-ferritin transcript. IREs serve as binding sites for iron regulatory proteins (IRPs), iron-sensing proteins that regulate ferritin translation. Previous observations suggested that each unique HHCS mutation conferred a characteristic degree of hyperferritinemia and cataract severity in affected individuals. Here we have measured the in vitro affinity of the IRPs for the mutant IREs and correlated decreases in binding affinity with clinical severity. Thermodynamic analysis of these IREs has also revealed that although some HHCS mutations lead to changes in the stability and secondary structure of the IRE, others appear to disrupt IRP-IRE recognition with minimal effect on IRE stability. HHCS is a noteworthy example of a human genetic disorder that arises from mutations within a protein-binding site of an mRNA cis-acting element. Analysis of the effects of these mutations on the energetics of the RNA-protein interaction explains the phenotypic variabilities of the disease state.  (+info)

Inborn errors of metabolism: iron. (2/114)

The iron content of the body is normally closely regulated. Despite this, iron deficiency anaemia is common in women because iron losses due to menstruation and childbirth are not always compensated for by iron absorption from the diet. The role of transferrin in delivering iron to cells and of ferritin in storing iron within cells is well understood but the proteins involved in iron transport across membranes are only now being investigated. Relatively few genetic disorders affecting iron metabolism are known and most are rare. This paper briefly describes pyridoxine responsive sideroblastic anaemia, hyperferritinaemia-cataract syndrome, atransferrinaemia and genetic haemochromatosis. Rather than rare, the latter is one of the most common inherited disorders in northern European populations. Mutations in genes regulating membrane iron transport causing simple iron deficiency have not yet been described.  (+info)

Survey of human mitochondrial diseases using new genomic/proteomic tools. (3/114)

BACKGROUND: We have constructed Bayesian prior-based, amino-acid sequence profiles for the complete yeast mitochondrial proteome and used them to develop methods for identifying and characterizing the context of protein mutations that give rise to human mitochondrial diseases. (Bayesian priors are conditional probabilities that allow the estimation of the likelihood of an event - such as an amino-acid substitution - on the basis of prior occurrences of similar events.) Because these profiles can assemble sets of taxonomically very diverse homologs, they enable identification of the structurally and/or functionally most critical sites in the proteins on the basis of the degree of sequence conservation. These profiles can also find distant homologs with determined three-dimensional structures that aid in the interpretation of effects of missense mutations. RESULTS: This survey reports such an analysis for 15 missense mutations, one insertion and three deletions involved in Leber's hereditary optic neuropathy, Leigh syndrome, mitochondrial neurogastrointestinal encephalomyopathy, Mohr-Tranebjaerg syndrome, iron-storage disorders related to Friedreich's ataxia, and hereditary spastic paraplegia. We present structural correlations for seven of the mutations. CONCLUSIONS: Of the 19 mutations analyzed, 14 involved changes in very highly conserved parts of the affected proteins. Five out of seven structural correlations provided reasonable explanations for the malfunctions. As additional genetic and structural data become available, this methodology can be extended. It has the potential for assisting in identifying new disease-related genes. Furthermore, profiles with structural homologs can generate mechanistic hypotheses concerning the underlying biochemical processes - and why they break down as a result of the mutations.  (+info)

Recent advances in disorders of iron metabolism: mutations, mechanisms and modifiers. (4/114)

The spectrum of known disorders of iron metabolism has expanded dramatically over the past few years. Identification of HFE, the gene most commonly mutated in patients with hereditary hemochromatosis, has allowed molecular diagnosis and paved the way for identification of other genes, such as TFR2, that are important in non-HFE-associated iron overload. There are clearly several other, unidentified, iron overload disease genes yet to be found. In parallel, our understanding of iron transport has expanded through identification of Fpn1/Ireg1/MTP1, Sfxn1 and DCYTB: Ongoing studies of Friedreich's ataxia, sideroblastic anemia, aceruloplasminemia and neurodegeneration with brain-iron accumulation are clarifying the role for iron in the nervous system. Finally, as the number of known iron metabolic genes increases and their respective functions are ascertained, new opportunities have arisen to identify genetic modifiers of iron homeostasis.  (+info)

Impaired retinal iron homeostasis associated with defective phagocytosis in Royal College of Surgeons rats. (5/114)

PURPOSE: To determine whether iron homeostasis disorder accompanies retinal degeneration in Royal College of Surgeons (RCS) rats. METHODS: The presence of iron was revealed directly by proton-induced X-ray emission (PIXE) and indirectly by electron microscopy (EM). Ferritin, transferrin (Tf), and transferrin receptor (Tf-R) were localized by immunohistochemistry. Ferritin and Tf proteins were analyzed by Western blot analysis. Comparative study of Tf-R content was performed by slot-blot analysis and ferritin content was evaluated by enzyme-linked immunosorbent assay (ELISA). Ferritin and Tf-R expression was studied by reverse transcription-polymerase chain reaction (RT-PCR) and Tf expression by in situ hybridization (ISH). All studies were performed in RCS and control retinas from postnatal days (PN)20 to PN55. RESULTS: PIXE analysis showed iron accumulation in outer retina of RCS rats in a time-dependent manner. EM studies revealed irregular iron inclusions on partially degenerated outer segments (OS) of photoreceptors and lamellar whorls at PN35 and very large iron deposits on membranes from a debris layer at PN55. No such deposits were found in the inner retina. Ferritin and Tf-R expression and protein levels seemed to be unaffected in the inner part of the retina. Iron accumulation was preceded by Tf degradation, as revealed by immunohistochemistry and Western blot analysis. Tf mRNA was detected in RCS rat retinal pigment epithelium (RPE) at all stages studied. CONCLUSIONS: This study presents the first evidence for a correlation of iron homeostasis imbalance with the neurodegenerative state of the retina in RCS rats. The iron imbalance is not the underlying genetic defect but is the result of impaired RPE-photoreceptor interaction, which leads to debris accumulation and subsequent blockage of the outer retina's iron delivery pathway. The increase of iron in the photoreceptor area may enhance the vulnerability of cells to oxidative stress.  (+info)

Ferritin crystal cataracts in hereditary hyperferritinemia cataract syndrome. (6/114)

PURPOSE: Hereditary hyperferritinemia cataract syndrome (HHCS) is a genetic disease defined by cataracts, hyperferritinemia, and ferritin light-chain (L-ferritin) gene mutations. HHCS was diagnosed in this study in one of the first families known to be affected in the United States, and the basis of lens opacities in HHCS was determined. METHODS: DNA amplification and sequencing of the human L-ferritin gene was used for mutation detection. RNA electrophoretic mobility shift analysis was performed to demonstrate functional consequences of a new mutation. Opacities were characterized by immunohistochemical and electron microscopic analyses of human HHCS lens aspirate. RESULTS: HHCS was diagnosed in five members of one family who had all three hallmark features: hyperferritinemia, a prominent cataract or history, and the finding of a novel mutation in the L-ferritin gene (C33T). This mutation interferes with function of the L-ferritin transcript in an RNA gel shift assay. Light-diffracting crystalline deposits were present in cataractous lenses from two affected family members but not in control lenses. Immunohistochemical analysis showed strong anti-L-ferritin reactivity in the crystalline deposits. Analysis of these deposits by transmission electron microscopy with fast Fourier transformation demonstrated macromolecular crystalline structure of the deposits. The data were consistent with a face-centered cubic crystal having a unit crystal cell size of 17 nm, both findings characteristic of ferritin crystals grown in vitro. CONCLUSIONS: HHCS cataract is due to numerous small opacities, predominantly in the lens cortex, that are light-diffracting ferritin crystals. Patients with HHCS may be recognized by a family history of cataracts and hyperferritinemia without increased serum iron.  (+info)

Glucose and oxygen hypometabolism in aceruloplasminemia brains. (7/114)

OBJECTIVE: Aceruloplasminemia is an iron metabolic disorder caused by mutations in the ceruloplasmin gene. It is characterized by progressive neurodegeneration in association with iron accumulation. Excess iron functions as a potent catalyst of biologic oxidation. Previously we showed that an increased iron concentration is associated with the products of lipid peroxidation in the serum, cerebrospinal fluid, and brain tissues. To clarify the free radical-mediated tissue injury caused by intracellular iron accumulation through mitochondrial dysfunction. PATIENTS AND METHODS: We have measure brain oxygen and glucose metabolisms using positron emission tomography (PET) and examined brains at autopsy for iron contents and activities of the mitochondrial respiratory chain in two affected patients who had different truncation mutations of the ceruloplasmin gene. RESULTS: PET showed a marked decrease in glucose and oxygen consumption in the entire brain of aceruloplasminemia patients, with a preponderance of metabolic reduction in basal ganglia. Enzyme activities in the mitochondrial respiratory chain of the basal ganglia were reduced to approximately 45% and 42% respectively for complexes I and IV. An inverse relationship was shown between the amounts of iron accumulated and the levels of mitochondrial enzyme activities in all the brain regions examined. CONCLUSION: Iron-mediated free radicals may contribute to the impairment of mitochondrial energy metabolism in aceruloplasminemia.  (+info)

Genetic disorders affecting proteins of iron and copper metabolism: clinical implications. (8/114)

Iron and copper are essential transition metals that permit the facile transfer of electrons in a series of critical biochemical pathways. Recent work has identified the specific proteins involved in the absorption, transport, utilization, and storage of iron and copper. Remarkable progress is being made in understanding the molecular basis of disorders of human iron and copper metabolism. This review describes these proteins and examines the clinical consequences of new insights into the pathophysiology of genetic abnormalities affecting iron and copper metabolisms. Hereditary hemochromatosis is the most common genetic disorder of iron metabolism caused by mutations in the HFE gene. Aceruloplasminemia is a rare iron metabolic disorder that results from deficiency of ceruloplasmin ferroxidase activity as a consequence of mutations in the ceruloplasmin gene. Menkes disease and Wilson's disease are inherited disorders of copper metabolism resulting from the absence or dysfunction of homologous copper-transporting ATPases.  (+info)

Iron metabolism disorders are a group of medical conditions that affect the body's ability to absorb, transport, store, or utilize iron properly. Iron is an essential nutrient that plays a crucial role in various bodily functions, including oxygen transportation and energy production. However, imbalances in iron levels can lead to several health issues.

There are two main types of iron metabolism disorders:

1. Iron deficiency anemia (IDA): This condition occurs when the body lacks adequate iron to produce sufficient amounts of hemoglobin, a protein in red blood cells responsible for carrying oxygen throughout the body. Causes of IDA may include inadequate dietary iron intake, blood loss, or impaired iron absorption due to conditions like celiac disease or inflammatory bowel disease.
2. Hemochromatosis: This is a genetic disorder characterized by excessive absorption and accumulation of iron in various organs, including the liver, heart, and pancreas. Over time, this excess iron can lead to organ damage and diseases such as cirrhosis, heart failure, diabetes, and arthritis. Hemochromatosis is typically caused by mutations in the HFE gene, which regulates iron absorption in the intestines.

Other iron metabolism disorders include:

* Anemia of chronic disease (ACD): A type of anemia that occurs in individuals with chronic inflammation or infection, where iron is not efficiently used for hemoglobin production due to altered regulation.
* Sideroblastic anemias: These are rare disorders characterized by the abnormal formation of ringed sideroblasts (immature red blood cells containing iron-laden mitochondria) in the bone marrow, leading to anemia and other symptoms.
* Iron-refractory iron deficiency anemia (IRIDA): A rare inherited disorder caused by mutations in the TMPRSS6 gene, resulting in impaired regulation of hepcidin, a hormone that controls iron absorption and distribution in the body. This leads to both iron deficiency and iron overload.

Proper diagnosis and management of iron metabolism disorders are essential to prevent complications and maintain overall health. Treatment options may include dietary modifications, iron supplementation, phlebotomy (bloodletting), or chelation therapy, depending on the specific disorder and its severity.

Lipid metabolism disorders are a group of conditions that result from abnormalities in the breakdown, transport, or storage of lipids (fats) in the body. These disorders can lead to an accumulation of lipids in various tissues and organs, causing them to function improperly.

There are several types of lipid metabolism disorders, including:

1. Hyperlipidemias: These are conditions characterized by high levels of cholesterol or triglycerides in the blood. They can increase the risk of cardiovascular disease and pancreatitis.
2. Hypercholesterolemia: This is a condition characterized by high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. It can increase the risk of cardiovascular disease.
3. Hypocholesterolemias: These are conditions characterized by low levels of cholesterol in the blood. Some of these disorders may be associated with an increased risk of cancer and neurological disorders.
4. Hypertriglyceridemias: These are conditions characterized by high levels of triglycerides in the blood. They can increase the risk of pancreatitis and cardiovascular disease.
5. Lipodystrophies: These are conditions characterized by abnormalities in the distribution of body fat, which can lead to metabolic abnormalities such as insulin resistance, diabetes, and high levels of triglycerides.
6. Disorders of fatty acid oxidation: These are conditions that affect the body's ability to break down fatty acids for energy, leading to muscle weakness, liver dysfunction, and in some cases, life-threatening neurological complications.

Lipid metabolism disorders can be inherited or acquired, and their symptoms and severity can vary widely depending on the specific disorder and the individual's overall health status. Treatment may include lifestyle changes, medications, and dietary modifications to help manage lipid levels and prevent complications.

Calcium metabolism disorders refer to a group of medical conditions that affect the body's ability to properly regulate the levels of calcium in the blood and tissues. Calcium is an essential mineral that plays a critical role in many bodily functions, including bone health, muscle contraction, nerve function, and blood clotting.

There are several types of calcium metabolism disorders, including:

1. Hypocalcemia: This is a condition characterized by low levels of calcium in the blood. It can be caused by various factors such as vitamin D deficiency, hypoparathyroidism, and certain medications. Symptoms may include muscle cramps, spasms, and tingling sensations in the fingers and toes.
2. Hypercalcemia: This is a condition characterized by high levels of calcium in the blood. It can be caused by various factors such as hyperparathyroidism, cancer, and certain medications. Symptoms may include fatigue, weakness, confusion, and kidney stones.
3. Osteoporosis: This is a condition characterized by weak and brittle bones due to low calcium levels in the bones. It can be caused by various factors such as aging, menopause, vitamin D deficiency, and certain medications. Symptoms may include bone fractures and loss of height.
4. Paget's disease: This is a condition characterized by abnormal bone growth and deformities due to disordered calcium metabolism. It can be caused by various factors such as genetics, age, and certain medications. Symptoms may include bone pain, fractures, and deformities.

Treatment for calcium metabolism disorders depends on the underlying cause of the condition. It may involve supplements, medication, dietary changes, or surgery. Proper diagnosis and management are essential to prevent complications such as kidney stones, bone fractures, and neurological damage.

In the context of medicine, iron is an essential micromineral and key component of various proteins and enzymes. It plays a crucial role in oxygen transport, DNA synthesis, and energy production within the body. Iron exists in two main forms: heme and non-heme. Heme iron is derived from hemoglobin and myoglobin in animal products, while non-heme iron comes from plant sources and supplements.

The recommended daily allowance (RDA) for iron varies depending on age, sex, and life stage:

* For men aged 19-50 years, the RDA is 8 mg/day
* For women aged 19-50 years, the RDA is 18 mg/day
* During pregnancy, the RDA increases to 27 mg/day
* During lactation, the RDA for breastfeeding mothers is 9 mg/day

Iron deficiency can lead to anemia, characterized by fatigue, weakness, and shortness of breath. Excessive iron intake may result in iron overload, causing damage to organs such as the liver and heart. Balanced iron levels are essential for maintaining optimal health.

Phosphorus metabolism disorders refer to a group of conditions that affect the body's ability to properly regulate the levels and utilization of phosphorus. Phosphorus is an essential mineral that plays a critical role in many biological processes, including energy production, bone formation, and nerve function.

Disorders of phosphorus metabolism can result from genetic defects, kidney dysfunction, vitamin D deficiency, or other medical conditions. These disorders can lead to abnormal levels of phosphorus in the blood, which can cause a range of symptoms, including muscle weakness, bone pain, seizures, and respiratory failure.

Examples of phosphorus metabolism disorders include:

1. Hypophosphatemia: This is a condition characterized by low levels of phosphorus in the blood. It can be caused by various factors, such as malnutrition, vitamin D deficiency, and kidney dysfunction.
2. Hyperphosphatemia: This is a condition characterized by high levels of phosphorus in the blood. It can be caused by kidney failure, tumor lysis syndrome, and certain medications.
3. Hereditary hypophosphatemic rickets: This is a genetic disorder that affects the body's ability to regulate vitamin D and phosphorus metabolism. It can lead to weakened bones and skeletal deformities.
4. Oncogenic osteomalacia: This is a rare condition that occurs when tumors produce substances that interfere with phosphorus metabolism, leading to bone pain and weakness.

Treatment for phosphorus metabolism disorders depends on the underlying cause of the disorder and may include dietary changes, supplements, medications, or surgery.

Metabolic diseases are a group of disorders caused by abnormal chemical reactions in your body's cells. These reactions are part of a complex process called metabolism, where your body converts the food you eat into energy.

There are several types of metabolic diseases, but they most commonly result from:

1. Your body not producing enough of certain enzymes that are needed to convert food into energy.
2. Your body producing too much of certain substances or toxins, often due to a genetic disorder.

Examples of metabolic diseases include phenylketonuria (PKU), diabetes, and gout. PKU is a rare condition where the body cannot break down an amino acid called phenylalanine, which can lead to serious health problems if left untreated. Diabetes is a common disorder that occurs when your body doesn't produce enough insulin or can't properly use the insulin it produces, leading to high blood sugar levels. Gout is a type of arthritis that results from too much uric acid in the body, which can form crystals in the joints and cause pain and inflammation.

Metabolic diseases can be inherited or acquired through environmental factors such as diet or lifestyle choices. Many metabolic diseases can be managed with proper medical care, including medication, dietary changes, and lifestyle modifications.

Glucose metabolism disorders are a group of conditions that result from abnormalities in the body's ability to produce, store, or use glucose, which is a simple sugar that serves as the primary source of energy for the body's cells. These disorders can be categorized into two main types: those caused by insufficient insulin production (such as type 1 diabetes) and those caused by impaired insulin action (such as type 2 diabetes).

In healthy individuals, glucose is absorbed from food during digestion and enters the bloodstream. The pancreas responds to this increase in blood glucose levels by releasing insulin, a hormone that signals cells throughout the body to take up glucose from the bloodstream and use it for energy production or storage.

Glucose metabolism disorders can disrupt this process at various stages, leading to high blood glucose levels (hyperglycemia) or low blood glucose levels (hypoglycemia). Some common examples of these disorders include:

1. Diabetes Mellitus: A group of metabolic disorders characterized by high blood glucose levels due to insufficient insulin production, impaired insulin action, or both. Type 1 diabetes results from the autoimmune destruction of pancreatic beta-cells that produce insulin, while type 2 diabetes is caused by a combination of insulin resistance and inadequate insulin secretion.
2. Gestational Diabetes: A form of high blood glucose that develops during pregnancy due to hormonal changes that impair insulin action.
3. Prediabetes: A condition where blood glucose levels are higher than normal but not yet high enough to be classified as diabetes.
4. Hypoglycemia: Abnormally low blood glucose levels, which can result from certain medications, hormonal deficiencies, or other medical conditions.
5. Glycogen Storage Diseases: A group of rare inherited metabolic disorders that affect the body's ability to store and break down glycogen, a complex carbohydrate that serves as an energy reserve in muscles and the liver.
6. Maturity-Onset Diabetes of the Young (MODY): A group of monogenic forms of diabetes caused by mutations in specific genes involved in insulin secretion or action.
7. Glucose Galactose Malabsorption: An inherited disorder that impairs the absorption of glucose and galactose, leading to severe diarrhea, dehydration, and high blood glucose levels.
8. Fructose Intolerance: A condition where the body cannot metabolize fructose properly due to a deficiency in the enzyme aldolase B, resulting in abdominal pain, diarrhea, and high blood glucose levels.

Iron chelating agents are medications that bind to iron in the body, forming a stable complex that can then be excreted from the body. These agents are primarily used to treat iron overload, a condition that can occur due to frequent blood transfusions or certain genetic disorders such as hemochromatosis. By reducing the amount of iron in the body, these medications can help prevent or reduce damage to organs such as the heart and liver. Examples of iron chelating agents include deferoxamine, deferasirox, and deferiprone.

Hepcidin is a peptide hormone primarily produced in the liver that plays a crucial role in regulating iron homeostasis within the body. It acts by inhibiting the absorption of dietary iron in the intestines and the release of iron from storage sites, such as macrophages, into the bloodstream. By reducing the amount of iron available for use, hepcidin helps prevent excessive iron accumulation in tissues, which can be harmful and contribute to the development of various diseases, including iron overload disorders and certain types of anemia. The production of hepcidin is regulated by several factors, including iron levels, inflammation, and erythropoiesis (the production of red blood cells).

Ferritin is a protein in iron-metabolizing cells that stores iron in a water-soluble form. It is found inside the cells (intracellular) and is released into the bloodstream when the cells break down or die. Measuring the level of ferritin in the blood can help determine the amount of iron stored in the body. High levels of ferritin may indicate hemochromatosis, inflammation, liver disease, or other conditions. Low levels of ferritin may indicate anemia, iron deficiency, or other conditions.

Iron overload is a condition characterized by an excessive accumulation of iron in the body's tissues and organs, particularly in the liver, heart, and pancreas. This occurs when the body absorbs more iron than it can use or eliminate, leading to iron levels that are higher than normal.

Iron overload can result from various factors, including hereditary hemochromatosis, a genetic disorder that affects how the body absorbs iron from food; frequent blood transfusions, which can cause iron buildup in people with certain chronic diseases such as sickle cell anemia or thalassemia; and excessive consumption of iron supplements or iron-rich foods.

Symptoms of iron overload may include fatigue, joint pain, abdominal discomfort, irregular heartbeat, and liver dysfunction. If left untreated, it can lead to serious complications such as cirrhosis, liver failure, diabetes, heart problems, and even certain types of cancer. Treatment typically involves regular phlebotomy (removal of blood) to reduce iron levels in the body, along with dietary modifications and monitoring by a healthcare professional.

Iron Regulatory Protein 1 (IRP1) is a protein that plays a crucial role in the post-transcriptional regulation of iron homeostasis in cells. It is involved in the detection of cellular iron levels and responds by modulating the translation and stability of messenger RNAs (mRNAs) that encode proteins essential for iron metabolism.

IRP1 can bind to specific sequences called Iron Responsive Elements (IREs) present in the untranslated regions of mRNAs. When cellular iron levels are low, IRP1 binds to IREs and inhibits the translation of mRNAs encoding proteins responsible for iron uptake and storage, while stabilizing mRNAs that encode proteins involved in iron mobilization. Conversely, when iron levels are high, IRP1 dissociates from IREs, allowing for the normal translation of these mRNAs and maintaining iron homeostasis within the cell.

It is important to note that IRP1 has dual functions: it can act as an Iron Regulatory Protein (IRP) when iron levels are low, and as a cytosolic aconitase (an enzyme in the citric acid cycle) when iron levels are sufficient. This ability to switch between these two roles is facilitated by the presence of a [4Fe-4S] cluster, which is sensitive to cellular iron levels. When iron is abundant, the [4Fe-4S] cluster assembles, converting IRP1 into its cytosolic aconitase form; when iron is scarce, the cluster disassembles, enabling IRP1 to bind IREs and regulate iron metabolism-related gene expression.

Iron Regulatory Protein 2 (IRP2) is a regulatory protein involved in the post-transcriptional control of iron homeostasis. It binds to specific sequences called Iron Responsive Elements (IREs) found in the untranslated regions of mRNAs encoding proteins involved in iron metabolism, such as ferritin and transferrin receptor.

When cellular iron levels are low, IRP2 binds to the IREs and prevents the degradation of iron-related mRNAs, leading to increased synthesis of iron uptake proteins and decreased synthesis of iron storage proteins. Conversely, when iron levels are high, IRP2 is degraded, allowing for the normal turnover and translation of these mRNAs.

IRP2 plays a crucial role in maintaining appropriate intracellular iron concentrations and protecting cells from iron-induced oxidative stress. Dysregulation of IRP2 has been implicated in various diseases, including anemia, neurodegenerative disorders, and cancer.

Iron-regulatory proteins (IRPs) are specialized RNA-binding proteins that play a crucial role in the post-transcriptional regulation of iron homeostasis in mammalian cells. They are named as such because they regulate the expression of genes involved in iron metabolism, primarily by binding to specific cis-acting elements known as iron-responsive elements (IREs) located within the untranslated regions (UTRs) of target mRNAs.

There are two main IRPs: IRP1 and IRP2. Both proteins contain an N-terminal RNA-binding domain that recognizes and binds to IREs, as well as a C-terminal region involved in protein-protein interactions and other regulatory functions. Under conditions of iron deficiency or oxidative stress, IRPs become activated and bind to IREs, leading to changes in mRNA stability, translation, or both.

IRP1 can exist in two distinct conformational states: an active RNA-binding form (when iron levels are low) and an inactive aconitase form (when iron levels are sufficient). In contrast, IRP2 is primarily regulated by protein degradation, with its stability being modulated by the presence or absence of iron.

By binding to IREs within mRNAs encoding proteins involved in iron uptake, storage, and utilization, IRPs help maintain cellular iron homeostasis through a variety of mechanisms, including:

1. Promoting translation of transferrin receptor 1 (TfR1) mRNA to increase iron import when iron levels are low.
2. Inhibiting translation of ferritin heavy chain and light chain mRNAs to reduce iron storage when iron levels are low.
3. Stabilizing the mRNA encoding divalent metal transporter 1 (DMT1) to enhance iron uptake under conditions of iron deficiency.
4. Promoting degradation of transferrin receptor 2 (TfR2) and ferroportin mRNAs to limit iron import and export, respectively, when iron levels are high.

Overall, the regulation of iron metabolism by IRPs is crucial for maintaining proper cellular function and preventing the accumulation of toxic free radicals generated by iron-catalyzed reactions.

Hemochromatosis is a medical condition characterized by excessive absorption and accumulation of iron in the body, resulting in damage to various organs. It's often referred to as "iron overload" disorder. There are two main types: primary (hereditary) and secondary (acquired). Primary hemochromatosis is caused by genetic mutations that lead to increased intestinal iron absorption, while secondary hemochromatosis can be the result of various conditions such as multiple blood transfusions, chronic liver disease, or certain types of anemia.

In both cases, the excess iron gets stored in body tissues, particularly in the liver, heart, and pancreas, which can cause organ damage and lead to complications like cirrhosis, liver failure, diabetes, heart problems, and skin discoloration. Early diagnosis and treatment through regular phlebotomy (blood removal) or chelation therapy can help manage the condition and prevent severe complications.

Transferrin receptors are membrane-bound proteins found on the surface of many cell types, including red and white blood cells, as well as various tissues such as the liver, brain, and placenta. These receptors play a crucial role in iron homeostasis by regulating the uptake of transferrin, an iron-binding protein, into the cells.

Transferrin binds to two ferric ions (Fe3+) in the bloodstream, forming a complex known as holo-transferrin. This complex then interacts with the transferrin receptors on the cell surface, leading to endocytosis of the transferrin-receptor complex into the cell. Once inside the cell, the acidic environment within the endosome causes the release of iron ions from the transferrin molecule, which can then be transported into the cytoplasm for use in various metabolic processes.

After releasing the iron, the apo-transferrin (iron-free transferrin) is recycled back to the cell surface and released back into the bloodstream, where it can bind to more ferric ions and repeat the cycle. This process helps maintain appropriate iron levels within the body and ensures that cells have access to the iron they need for essential functions such as DNA synthesis, energy production, and oxygen transport.

In summary, transferrin receptors are membrane-bound proteins responsible for recognizing and facilitating the uptake of transferrin-bound iron into cells, playing a critical role in maintaining iron homeostasis within the body.

Transferrin is a glycoprotein that plays a crucial role in the transport and homeostasis of iron in the body. It's produced mainly in the liver and has the ability to bind two ferric (Fe3+) ions in its N-lobe and C-lobe, thus creating transferrin saturation.

This protein is essential for delivering iron to cells while preventing the harmful effects of free iron, which can catalyze the formation of reactive oxygen species through Fenton reactions. Transferrin interacts with specific transferrin receptors on the surface of cells, particularly in erythroid precursors and brain endothelial cells, to facilitate iron uptake via receptor-mediated endocytosis.

In addition to its role in iron transport, transferrin also has antimicrobial properties due to its ability to sequester free iron, making it less available for bacterial growth and survival. Transferrin levels can be used as a clinical marker of iron status, with decreased levels indicating iron deficiency anemia and increased levels potentially signaling inflammation or liver disease.

Antimicrobial cationic peptides (ACPs) are a group of small, naturally occurring peptides that possess broad-spectrum antimicrobial activity against various microorganisms, including bacteria, fungi, viruses, and parasites. They are called "cationic" because they contain positively charged amino acid residues (such as lysine and arginine), which allow them to interact with and disrupt the negatively charged membranes of microbial cells.

ACPs are produced by a wide range of organisms, including humans, animals, and plants, as part of their innate immune response to infection. They play an important role in protecting the host from invading pathogens by directly killing them or inhibiting their growth.

The antimicrobial activity of ACPs is thought to be mediated by their ability to disrupt the membranes of microbial cells, leading to leakage of cellular contents and death. Some ACPs may also have intracellular targets, such as DNA or protein synthesis, that contribute to their antimicrobial activity.

ACPs are being studied for their potential use as therapeutic agents to treat infectious diseases, particularly those caused by drug-resistant bacteria. However, their clinical application is still in the early stages of development due to concerns about their potential toxicity to host cells and the emergence of resistance mechanisms in microbial pathogens.

Dietary iron is a vital nutrient that plays a crucial role in the production of hemoglobin, a protein in red blood cells responsible for carrying oxygen throughout the body. It is also essential for various other bodily functions, including energy production and immune function.

There are two forms of dietary iron: heme and non-heme. Heme iron is found in animal products such as meat, poultry, and fish, while non-heme iron is found in plant-based foods such as beans, lentils, tofu, spinach, and fortified cereals.

The recommended daily intake of dietary iron varies depending on age, sex, and other factors. For example, adult men typically require 8 milligrams (mg) per day, while adult women need 18 mg per day. Pregnant women may require up to 27 mg per day, while breastfeeding women need around 9-10 mg per day.

It is important to note that the absorption of non-heme iron from plant-based foods can be enhanced by consuming them with vitamin C-rich foods or drinks, such as citrus fruits, strawberries, and bell peppers. On the other hand, certain substances such as tannins (found in tea and coffee) and phytates (found in whole grains and legumes) can inhibit the absorption of non-heme iron.

I must clarify that "Iron Isotopes" is not a medical term, but rather a scientific concept from the field of physics and chemistry. However, I can certainly provide a general explanation of isotopes and then focus on iron isotopes specifically.

An isotope is a variant of a chemical element that has the same number of protons (and thus the same atomic number) but a different number of neutrons within its nucleus. This results in variations of the atomic mass of isotopes of the same element. Some isotopes are stable, while others are unstable and will decay over time into other elements or isotopes, a process called radioactive decay.

Iron (Fe) has four naturally occurring stable isotopes: Fe-54, Fe-56, Fe-57, and Fe-58. These iron isotopes have different numbers of neutrons in their nuclei, resulting in slightly different atomic masses. The most abundant iron isotope is Fe-56, which contains 26 protons and 30 neutrons in its nucleus.

In the context of human health, iron is an essential nutrient that plays a crucial role in various biological processes, such as oxygen transport and energy production. However, the concept of iron isotopes does not have a direct medical relevance, but it can be useful in scientific research related to fields like geochemistry, environmental science, or nuclear physics.

Iron-deficiency anemia is a condition characterized by a decrease in the total amount of hemoglobin or red blood cells in the blood, caused by insufficient iron levels in the body. Hemoglobin is a protein in red blood cells that carries oxygen from the lungs to the rest of the body. When iron levels are low, the body cannot produce enough hemoglobin, leading to the production of smaller and fewer red blood cells, known as microcytic hypochromic anemia.

Iron is essential for the production of hemoglobin, and a deficiency in iron can result from inadequate dietary intake, chronic blood loss, or impaired absorption. In addition to fatigue and weakness, symptoms of iron-deficiency anemia may include shortness of breath, headaches, dizziness, pale skin, and brittle nails. Treatment typically involves iron supplementation and addressing the underlying cause of the iron deficiency.

Cation transport proteins are a type of membrane protein that facilitate the movement of cations (positively charged ions) across biological membranes. These proteins play a crucial role in maintaining ion balance and electrical excitability within cells, as well as in various physiological processes such as nutrient uptake, waste elimination, and signal transduction.

There are several types of cation transport proteins, including:

1. Ion channels: These are specialized protein structures that form a pore or channel through the membrane, allowing ions to pass through rapidly and selectively. They can be either voltage-gated or ligand-gated, meaning they open in response to changes in electrical potential or binding of specific molecules, respectively.

2. Ion pumps: These are active transport proteins that use energy from ATP hydrolysis to move ions against their electrochemical gradient, effectively pumping them from one side of the membrane to the other. Examples include the sodium-potassium pump (Na+/K+-ATPase) and calcium pumps (Ca2+ ATPase).

3. Ion exchangers: These are antiporter proteins that facilitate the exchange of one ion for another across the membrane, maintaining electroneutrality. For example, the sodium-proton exchanger (NHE) moves a proton into the cell in exchange for a sodium ion being moved out.

4. Symporters: These are cotransporter proteins that move two or more ions together in the same direction, often coupled with the transport of a solute molecule. An example is the sodium-glucose cotransporter (SGLT), which facilitates glucose uptake into cells by coupling its movement with that of sodium ions.

Collectively, cation transport proteins help maintain ion homeostasis and contribute to various cellular functions, including electrical signaling, enzyme regulation, and metabolic processes. Dysfunction in these proteins can lead to a range of diseases, such as neurological disorders, cardiovascular disease, and kidney dysfunction.

"Iron radioisotopes" refer to specific forms of the element iron that have unstable nuclei and emit radiation. These isotopes are often used in medical imaging and treatment procedures due to their ability to be detected by specialized equipment. Common iron radioisotopes include Iron-52, Iron-55, Iron-59, and Iron-60. They can be used as tracers to study the distribution, metabolism, or excretion of iron in the body, or for targeted radiation therapy in conditions such as cancer.

Iron-binding proteins, also known as transferrins, are a type of protein responsible for the transport and storage of iron in the body. They play a crucial role in maintaining iron homeostasis by binding free iron ions and preventing them from participating in harmful chemical reactions that can produce reactive oxygen species (ROS) and cause cellular damage.

Transferrin is the primary iron-binding protein found in blood plasma, while lactoferrin is found in various exocrine secretions such as milk, tears, and saliva. Both transferrin and lactoferrin have a similar structure, consisting of two lobes that can bind one ferric ion (Fe3+) each. When iron is bound to these proteins, they are called holo-transferrin or holo-lactoferrin; when they are unbound, they are referred to as apo-transferrin or apo-lactoferrin.

Iron-binding proteins have a high affinity for iron and can regulate the amount of free iron available in the body. They help prevent iron overload, which can lead to oxidative stress and cellular damage, as well as iron deficiency, which can result in anemia and other health problems.

In summary, iron-binding proteins are essential for maintaining iron homeostasis by transporting and storing iron ions, preventing them from causing harm to the body's cells.

Apoferritins are the protein shells or apoproteins of ferritin molecules that are devoid of iron. Ferritin is a protein in cells that stores iron and releases it in a form that can be used by the body. Apoferritin can bind with iron ions to form ferritin. It has a hollow, spherical structure and is often used as a model for studying protein folding and assembly.

Ceruloplasmin is a protein found in blood plasma that binds and transports copper ions. It plays a crucial role in copper metabolism, including the oxidation of ferrous iron to ferric iron, which is necessary for the incorporation of iron into transferrin, another protein responsible for transporting iron throughout the body. Ceruloplasmin also acts as an antioxidant by scavenging free radicals and has been implicated in neurodegenerative disorders like Alzheimer's disease and Wilson's disease, a genetic disorder characterized by abnormal copper accumulation in various organs.

Bipolar disorder, also known as manic-depressive illness, is a mental health condition that causes extreme mood swings that include emotional highs (mania or hypomania) and lows (depression). When you become depressed, you may feel sad or hopeless and lose interest or pleasure in most activities. When your mood shifts to mania or hypomania (a less severe form of mania), you may feel euphoric, full of energy, or unusually irritable. These mood swings can significantly affect your job, school, relationships, and overall quality of life.

Bipolar disorder is typically characterized by the presence of one or more manic or hypomanic episodes, often accompanied by depressive episodes. The episodes may be separated by periods of normal mood, but in some cases, a person may experience rapid cycling between mania and depression.

There are several types of bipolar disorder, including:

* Bipolar I Disorder: This type is characterized by the occurrence of at least one manic episode, which may be preceded or followed by hypomanic or major depressive episodes.
* Bipolar II Disorder: This type involves the presence of at least one major depressive episode and at least one hypomanic episode, but no manic episodes.
* Cyclothymic Disorder: This type is characterized by numerous periods of hypomania and depression that are not severe enough to meet the criteria for a full manic or depressive episode.
* Other Specified and Unspecified Bipolar and Related Disorders: These categories include bipolar disorders that do not fit the criteria for any of the other types.

The exact cause of bipolar disorder is unknown, but it appears to be related to a combination of genetic, environmental, and neurochemical factors. Treatment typically involves a combination of medication, psychotherapy, and lifestyle changes to help manage symptoms and prevent relapses.

Deferoxamine is a medication used to treat iron overload, which can occur due to various reasons such as frequent blood transfusions or excessive iron intake. It works by binding to excess iron in the body and promoting its excretion through urine. This helps to prevent damage to organs such as the heart and liver that can be caused by high levels of iron.

Deferoxamine is an injectable medication that is typically administered intravenously or subcutaneously, depending on the specific regimen prescribed by a healthcare professional. It may also be used in combination with other medications to manage iron overload more effectively.

It's important to note that deferoxamine should only be used under the guidance of a medical professional, as improper use or dosing can lead to serious side effects or complications.

Aconitate hydratase is an enzyme that catalyzes the reversible conversion of citrate to isocitrate in the Krebs cycle (also known as the tricarboxylic acid cycle or TCA cycle), which is a central metabolic pathway in the cell. This enzyme is also called aconitase or aconitate dehydratase.

The reaction catalyzed by aconitate hydratase involves two steps: first, the removal of a water molecule from citrate to form cis-aconitate; and second, the addition of a water molecule to cis-aconitate to form isocitrate. The enzyme binds to the substrate in such a way that it stabilizes the transition state between citrate and cis-aconitate, making the reaction more favorable.

Aconitate hydratase plays an important role in energy metabolism, as it helps generate NADH and FADH2, which are used to produce ATP through oxidative phosphorylation. Additionally, aconitate hydratase has been implicated in various diseases, including neurodegenerative disorders, cancer, and bacterial infections.

Ferric compounds are inorganic compounds that contain the iron(III) cation, Fe3+. Iron(III) is a transition metal and can form stable compounds with various anions. Ferric compounds are often colored due to the d-d transitions of the iron ion. Examples of ferric compounds include ferric chloride (FeCl3), ferric sulfate (Fe2(SO4)3), and ferric oxide (Fe2O3). Ferric compounds have a variety of uses, including as catalysts, in dye production, and in medical applications.

Energy metabolism is the process by which living organisms produce and consume energy to maintain life. It involves a series of chemical reactions that convert nutrients from food, such as carbohydrates, fats, and proteins, into energy in the form of adenosine triphosphate (ATP).

The process of energy metabolism can be divided into two main categories: catabolism and anabolism. Catabolism is the breakdown of nutrients to release energy, while anabolism is the synthesis of complex molecules from simpler ones using energy.

There are three main stages of energy metabolism: glycolysis, the citric acid cycle (also known as the Krebs cycle), and oxidative phosphorylation. Glycolysis occurs in the cytoplasm of the cell and involves the breakdown of glucose into pyruvate, producing a small amount of ATP and nicotinamide adenine dinucleotide (NADH). The citric acid cycle takes place in the mitochondria and involves the further breakdown of pyruvate to produce more ATP, NADH, and carbon dioxide. Oxidative phosphorylation is the final stage of energy metabolism and occurs in the inner mitochondrial membrane. It involves the transfer of electrons from NADH and other electron carriers to oxygen, which generates a proton gradient across the membrane. This gradient drives the synthesis of ATP, producing the majority of the cell's energy.

Overall, energy metabolism is a complex and essential process that allows organisms to grow, reproduce, and maintain their bodily functions. Disruptions in energy metabolism can lead to various diseases, including diabetes, obesity, and neurodegenerative disorders.

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.

Iron-sulfur proteins are a group of metalloproteins that contain iron and sulfur atoms in their active centers. These clusters of iron and sulfur atoms, also known as iron-sulfur clusters, can exist in various forms, including Fe-S, 2Fe-2S, 3Fe-4S, and 4Fe-4S structures. The iron atoms are coordinated to the protein through cysteine residues, while the sulfur atoms can be in the form of sulfide (S2-) or sulfane (-S-).

These proteins play crucial roles in many biological processes, such as electron transfer, redox reactions, and enzyme catalysis. They are found in various organisms, from bacteria to humans, and are involved in a wide range of cellular functions, including energy metabolism, photosynthesis, nitrogen fixation, and DNA repair.

Iron-sulfur proteins can be classified into several categories based on their structure and function, such as ferredoxins, Rieske proteins, high-potential iron-sulfur proteins (HiPIPs), and radical SAM enzymes. Dysregulation or mutations in iron-sulfur protein genes have been linked to various human diseases, including neurodegenerative disorders, cancer, and mitochondrial disorders.

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

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

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

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

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.

Hypochromic anemia is a type of anemia characterized by the presence of red blood cells that have lower than normal levels of hemoglobin and appear paler in color than normal. Hemoglobin is a protein in red blood cells that carries oxygen from the lungs to the rest of the body. In hypochromic anemia, there may be a decrease in the production or increased destruction of red blood cells, leading to a reduced number of red blood cells and insufficient oxygen supply to the tissues.

Hypochromic anemia can result from various underlying medical conditions, including iron deficiency, thalassemia, chronic inflammation, lead poisoning, and certain infections or chronic diseases. Treatment for hypochromic anemia depends on the underlying cause and may include iron supplements, dietary changes, medications, or blood transfusions.

A mental disorder is a syndrome characterized by clinically significant disturbance in an individual's cognition, emotion regulation, or behavior. It's associated with distress and/or impaired functioning in social, occupational, or other important areas of life, often leading to a decrease in quality of life. These disorders are typically persistent and can be severe and disabling. They may be related to factors such as genetics, early childhood experiences, or trauma. Examples include depression, anxiety disorders, bipolar disorder, schizophrenia, and personality disorders. It's important to note that a diagnosis should be made by a qualified mental health professional.

Flavin Mononucleotide (FMN) Reductase is an enzyme that catalyzes the reduction of FMN to FMNH2 using NADH or NADPH as an electron donor. This enzyme plays a crucial role in the electron transport chain and is involved in various redox reactions within the cell. It is found in many organisms, including bacteria, fungi, plants, and animals. In humans, FMN Reductase is encoded by the RIBFLR gene and is primarily located in the mitochondria. Defects in this enzyme can lead to various metabolic disorders.

Siderophores are low-molecular-weight organic compounds that are secreted by microorganisms, such as bacteria and fungi, to chelate and solubilize iron from their environment. They are able to bind ferric iron (Fe3+) with very high affinity and form a siderophore-iron complex, which can then be taken up by the microorganism through specific transport systems. This allows them to acquire iron even in environments where it is present at very low concentrations or in forms that are not readily available for uptake. Siderophores play an important role in the survival and virulence of many pathogenic microorganisms, as they help them to obtain the iron they need to grow and multiply.

Anxiety disorders are a category of mental health disorders characterized by feelings of excessive and persistent worry, fear, or anxiety that interfere with daily activities. They include several different types of disorders, such as:

1. Generalized Anxiety Disorder (GAD): This is characterized by chronic and exaggerated worry and tension, even when there is little or nothing to provoke it.
2. Panic Disorder: This is characterized by recurring unexpected panic attacks and fear of experiencing more panic attacks.
3. Social Anxiety Disorder (SAD): Also known as social phobia, this is characterized by excessive fear, anxiety, or avoidance of social situations due to feelings of embarrassment, self-consciousness, and concern about being judged or viewed negatively by others.
4. Phobias: These are intense, irrational fears of certain objects, places, or situations. When a person with a phobia encounters the object or situation they fear, they may experience panic attacks or other severe anxiety responses.
5. Agoraphobia: This is a fear of being in places where it may be difficult to escape or get help if one has a panic attack or other embarrassing or incapacitating symptoms.
6. Separation Anxiety Disorder (SAD): This is characterized by excessive anxiety about separation from home or from people to whom the individual has a strong emotional attachment (such as a parent, sibling, or partner).
7. Selective Mutism: This is a disorder where a child becomes mute in certain situations, such as at school, but can speak normally at home or with close family members.

These disorders are treatable with a combination of medication and psychotherapy (cognitive-behavioral therapy, exposure therapy). It's important to seek professional help if you suspect that you or someone you know may have an anxiety disorder.

Mood disorders are a category of mental health disorders characterized by significant and persistent changes in mood, affect, and emotional state. These disorders can cause disturbances in normal functioning and significantly impair an individual's ability to carry out their daily activities. The two primary types of mood disorders are depressive disorders (such as major depressive disorder or persistent depressive disorder) and bipolar disorders (which include bipolar I disorder, bipolar II disorder, and cyclothymic disorder).

Depressive disorders involve prolonged periods of low mood, sadness, hopelessness, and a lack of interest in activities. Individuals with these disorders may also experience changes in sleep patterns, appetite, energy levels, concentration, and self-esteem. In severe cases, they might have thoughts of death or suicide.

Bipolar disorders involve alternating episodes of mania (or hypomania) and depression. During a manic episode, individuals may feel extremely elated, energetic, or irritable, with racing thoughts, rapid speech, and impulsive behavior. They might engage in risky activities, have decreased sleep needs, and display poor judgment. In contrast, depressive episodes involve the same symptoms as depressive disorders.

Mood disorders can be caused by a combination of genetic, biological, environmental, and psychological factors. Proper diagnosis and treatment, which may include psychotherapy, medication, or a combination of both, are essential for managing these conditions and improving quality of life.

Ferrous compounds are inorganic substances that contain iron (Fe) in its +2 oxidation state. The term "ferrous" is derived from the Latin word "ferrum," which means iron. Ferrous compounds are often used in medicine, particularly in the treatment of iron-deficiency anemia due to their ability to provide bioavailable iron to the body.

Examples of ferrous compounds include ferrous sulfate, ferrous gluconate, and ferrous fumarate. These compounds are commonly found in dietary supplements and multivitamins. Ferrous sulfate is one of the most commonly used forms of iron supplementation, as it has a high iron content and is relatively inexpensive.

It's important to note that ferrous compounds can be toxic in large doses, so they should be taken under the guidance of a healthcare professional. Overdose can lead to symptoms such as nausea, vomiting, diarrhea, abdominal pain, and potentially fatal consequences if left untreated.

Hemoglobin (Hb or Hgb) is the main oxygen-carrying protein in the red blood cells, which are responsible for delivering oxygen throughout the body. It is a complex molecule made up of four globin proteins and four heme groups. Each heme group contains an iron atom that binds to one molecule of oxygen. Hemoglobin plays a crucial role in the transport of oxygen from the lungs to the body's tissues, and also helps to carry carbon dioxide back to the lungs for exhalation.

There are several types of hemoglobin present in the human body, including:

* Hemoglobin A (HbA): This is the most common type of hemoglobin, making up about 95-98% of total hemoglobin in adults. It consists of two alpha and two beta globin chains.
* Hemoglobin A2 (HbA2): This makes up about 1.5-3.5% of total hemoglobin in adults. It consists of two alpha and two delta globin chains.
* Hemoglobin F (HbF): This is the main type of hemoglobin present in fetal life, but it persists at low levels in adults. It consists of two alpha and two gamma globin chains.
* Hemoglobin S (HbS): This is an abnormal form of hemoglobin that can cause sickle cell disease when it occurs in the homozygous state (i.e., both copies of the gene are affected). It results from a single amino acid substitution in the beta globin chain.
* Hemoglobin C (HbC): This is another abnormal form of hemoglobin that can cause mild to moderate hemolytic anemia when it occurs in the homozygous state. It results from a different single amino acid substitution in the beta globin chain than HbS.

Abnormal forms of hemoglobin, such as HbS and HbC, can lead to various clinical disorders, including sickle cell disease, thalassemia, and other hemoglobinopathies.

Inborn errors of metal metabolism refer to genetic disorders that affect the way the body processes and handles certain metallic elements. These disorders can result in an accumulation or deficiency of specific metals, leading to various clinical manifestations. Examples of such conditions include:

1. Wilson's disease: An autosomal recessive disorder caused by a mutation in the ATP7B gene, which results in abnormal copper metabolism and accumulation in various organs, particularly the liver and brain.
2. Menkes disease: An X-linked recessive disorder caused by a mutation in the ATP7A gene, leading to impaired copper transport and deficiency, affecting the brain, bones, and connective tissue.
3. Hemochromatosis: An autosomal recessive disorder characterized by excessive iron absorption and deposition in various organs, causing damage to the liver, heart, and pancreas.
4. Acrodermatitis enteropathica: A rare autosomal recessive disorder caused by a mutation in the SLC39A4 gene, resulting in zinc deficiency and affecting the skin, gastrointestinal system, and immune function.
5. Disturbances in manganese metabolism: Rare genetic disorders that can lead to either manganese accumulation or deficiency, causing neurological symptoms.

These conditions often require specialized medical management, including dietary modifications, chelation therapy, and/or supplementation to maintain appropriate metal homeostasis and prevent organ damage.

Erythropoiesis is the process of forming and developing red blood cells (erythrocytes) in the body. It occurs in the bone marrow and is regulated by the hormone erythropoietin (EPO), which is produced by the kidneys. Erythropoiesis involves the differentiation and maturation of immature red blood cell precursors called erythroblasts into mature red blood cells, which are responsible for carrying oxygen to the body's tissues. Disorders that affect erythropoiesis can lead to anemia or other blood-related conditions.

Iron compounds refer to chemical substances that contain iron (Fe) combined with other elements. Iron is an essential mineral for the human body, playing a crucial role in various bodily functions such as oxygen transport, DNA synthesis, and energy production.

There are several types of iron compounds, including:

1. Inorganic iron salts: These are commonly used in dietary supplements and fortified foods to treat or prevent iron deficiency anemia. Examples include ferrous sulfate, ferrous gluconate, and ferric iron.
2. Heme iron: This is the form of iron found in animal products such as meat, poultry, and fish. It is more easily absorbed by the body compared to non-heme iron from plant sources.
3. Non-heme iron: This is the form of iron found in plant-based foods such as grains, legumes, fruits, and vegetables. It is not as well-absorbed as heme iron but can be enhanced by consuming it with vitamin C or other organic acids.

It's important to note that excessive intake of iron compounds can lead to iron toxicity, which can cause serious health problems. Therefore, it's essential to follow recommended dosages and consult a healthcare professional before taking any iron supplements.

Anemia is a medical condition characterized by a lower than normal number of red blood cells or lower than normal levels of hemoglobin in the blood. Hemoglobin is an important protein in red blood cells that carries oxygen from the lungs to the rest of the body. Anemia can cause fatigue, weakness, shortness of breath, and a pale complexion because the body's tissues are not getting enough oxygen.

Anemia can be caused by various factors, including nutritional deficiencies (such as iron, vitamin B12, or folate deficiency), blood loss, chronic diseases (such as kidney disease or rheumatoid arthritis), inherited genetic disorders (such as sickle cell anemia or thalassemia), and certain medications.

There are different types of anemia, classified based on the underlying cause, size and shape of red blood cells, and the level of hemoglobin in the blood. Treatment for anemia depends on the underlying cause and may include dietary changes, supplements, medication, or blood transfusions.

Heme is not a medical term per se, but it is a term used in the field of medicine and biology. Heme is a prosthetic group found in hemoproteins, which are proteins that contain a heme iron complex. This complex plays a crucial role in various biological processes, including oxygen transport (in hemoglobin), electron transfer (in cytochromes), and chemical catalysis (in peroxidases and catalases).

The heme group consists of an organic component called a porphyrin ring, which binds to a central iron atom. The iron atom can bind or release electrons, making it essential for redox reactions in the body. Heme is also vital for the formation of hemoglobin and myoglobin, proteins responsible for oxygen transport and storage in the blood and muscles, respectively.

In summary, heme is a complex organic-inorganic structure that plays a critical role in several biological processes, particularly in electron transfer and oxygen transport.

The Diagnostic and Statistical Manual of Mental Disorders (DSM) is a publication of the American Psychiatric Association (APA) that provides diagnostic criteria for mental disorders. It is widely used by mental health professionals in the United States and around the world to diagnose and classify mental health conditions.

The DSM includes detailed descriptions of symptoms, clinical examples, and specific criteria for each disorder, which are intended to facilitate accurate diagnosis and improve communication among mental health professionals. The manual is regularly updated to reflect current research and clinical practice, with the most recent edition being the DSM-5, published in 2013.

It's important to note that while the DSM is a valuable tool for mental health professionals, it is not without controversy. Some critics argue that the manual medicalizes normal human experiences and that its categories may be too broad or overlapping. Nonetheless, it remains an essential resource for clinicians, researchers, and policymakers in the field of mental health.

Membrane proteins are a type of protein that are embedded in the lipid bilayer of biological membranes, such as the plasma membrane of cells or the inner membrane of mitochondria. These proteins play crucial roles in various cellular processes, including:

1. Cell-cell recognition and signaling
2. Transport of molecules across the membrane (selective permeability)
3. Enzymatic reactions at the membrane surface
4. Energy transduction and conversion
5. Mechanosensation and signal transduction

Membrane proteins can be classified into two main categories: integral membrane proteins, which are permanently associated with the lipid bilayer, and peripheral membrane proteins, which are temporarily or loosely attached to the membrane surface. Integral membrane proteins can further be divided into three subcategories based on their topology:

1. Transmembrane proteins, which span the entire width of the lipid bilayer with one or more alpha-helices or beta-barrels.
2. Lipid-anchored proteins, which are covalently attached to lipids in the membrane via a glycosylphosphatidylinositol (GPI) anchor or other lipid modifications.
3. Monotopic proteins, which are partially embedded in the membrane and have one or more domains exposed to either side of the bilayer.

Membrane proteins are essential for maintaining cellular homeostasis and are targets for various therapeutic interventions, including drug development and gene therapy. However, their structural complexity and hydrophobicity make them challenging to study using traditional biochemical methods, requiring specialized techniques such as X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and single-particle cryo-electron microscopy (cryo-EM).

Human iron metabolism Iron deficiency anemia Roy CN, Andrews NC (October 2001). "Recent advances in disorders of iron ... Iron metabolism disorders may involve a number of genes including HFE and TFR2. Hepcidin is the master regulator of iron ... http://sickle.bwh.harvard.edu/menu_iron.html Andrews NC (December 1999). "Disorders of iron metabolism". N. Engl. J. Med. 341 ( ... So though many mysteries of iron metabolism remain, the discovery of hepcidin already allows a much better understanding of the ...
Andrews N (1999). "Disorders of iron metabolism". New England Journal of Medicine. 341 (26): 1986-95. doi:10.1056/ ... Iron metabolism, Genetic disorders with OMIM but no gene, Hepatology, Rare diseases). ... Its characteristics are similar to hereditary hemochromatosis, where iron deposition causes damage to the liver and other ...
Harvey JW (2008). "Iron Metabolism and Its Disorders". Clinical Biochemistry of Domestic Animals. Elsevier. pp. 259-285. doi: ... Iron within the heme group must be in the Fe+2 state to bind oxygen. If iron is oxidized to the Fe+3 state, metmyoglobin is ... If meat has been exposed to nitrites, it will remain pink, because the iron atom is bound to NO, nitric oxide (true of, e.g., ... The oxygen atoms are colored in green, the iron atom is colored in red, and the heme group is colored in blue. Many models of ...
Medical Progress: Disorders of Iron Metabolism. New England Journal of Medicine 1999;341:1986-95. Donovan A, Brownlie A, Zhou Y ... The iron exporter ferroportin (Slc40a1) is essential for iron homeostasis. Cell Metabolism 2005; 1:191-200. Gunshin H, Fujiwara ... Mutations in TMPRSS6 cause iron-refractory, iron deficiency anemia. Nature Genetics 2008; 40:569-571. Xu W, Barrientos T, Mao L ... Andrews studied treatments for and molecular processes governing iron disease, such as anemia (iron deficiency) and ...
Bohn, Andrea A. (November 2013). "Diagnosis of disorders of iron metabolism in dogs and cats". The Veterinary Clinics of North ... Maintaining an optimum ratio allows for the continued tight regulation of calcium metabolism, which is important to many normal ... "Nutritional consequences of interspecies differences in arginine and lysine metabolism". The Journal of Nutrition. 137 (6 Suppl ...
... and antioxidant factors in iron and porphyrin metabolism disorders". Italian Journal of Gastroenterology and Hepatology. 31 (9 ... Additional risk factors include alcohol use disorder, excess iron (from iron supplements as well as cooking on cast iron ... Certain mutations in the HFE gene cause hemochromatosis (an iron overload disorder). People who have these mutations are also ... A borderline iron deficiency has been found to have a protective effect by limiting heme synthesis. In the absence of iron, ...
Human iron metabolism Iron overload disorder "Aceruloplasminemia , Genetic and Rare Diseases Information Center (GARD) - an ... Inborn errors of metal metabolism, Hepatology, Autosomal recessive disorders, Iron metabolism). ... molecular characterization of this disorder of iron metabolism". Proceedings of the National Academy of Sciences of the United ... Iron accumulation in the tissues and organs results in a corresponding iron deficiency in the blood, leading to anemia. Anemia ...
Human iron metabolism Iron deficiency Hsu CC, Senussi NH, Fertrin KY, Kowdley KV (June 2022). "Iron overload disorders". ... The human diet contains iron in two forms: heme iron and non-heme iron. Heme iron is usually found in red meat, whereas non- ... metabolism: diabetes in people with iron overload occurs as a result of selective iron deposition in islet beta cells in the ... Andrews, Nancy C. (1999). "Disorders of Iron Metabolism". New England Journal of Medicine. 341 (26): 1986-95. doi:10.1056/ ...
Conrad ME, Umbreit JN (Apr 2000). "Disorders of iron metabolism". The New England Journal of Medicine. 342 (17): 1293-4. doi: ... The ubiquity of Iron in life has led to the Iron-sulfur world hypothesis that Iron was a central component of the environment ... The ferritin storage iron pool is much larger than the labile iron pool, ranging in concentration from 0.7 mM to 3.6 mM. Iron ... Iron can also be oxidized by marine microbes under conditions that are high in iron and low in oxygen. Iron can enter marine ...
A comprehensive NIH factsheet on iron and nutrition Iron Disorders Institute: A nonprofit group concerned with iron disorders; ... Iron in biology Conrad ME, Umbreit JN (Apr 2000). "Disorders of iron metabolism". The New England Journal of Medicine. 342 (17 ... However, some of the intracellular iron is bound to low-affinity complexes, and is termed labile iron or "free" iron. Iron in ... because iron is essential for red blood cells, where most of the human body's iron is contained. Understanding iron metabolism ...
... disorders of iron metabolism and Tay-Sachs disease. He was also among the first scientists to identify X-inactivation as the ... Iron metabolism. Annu Rev Med 12: 195-210, 1961 Beutler,E. Erythrocyte carbohydrate metabolism. In: Weinstein,I.M.; Beutler,E ... where he studied iron metabolism and red blood cell metabolism. In 1959, he became chairman of the Department of Medicine of ... Iron Metabolism Berlin: Springer-Verlag; 1963: 256-262. Beutler, E. The hemolytic effect of primaquine and related compounds. A ...
... disorders of iron metabolism and Tay-Sachs disease. Richard Kekuni Blaisdell, class of 1948, professor emeritus of medicine at ...
Iron metabolism, Diseases and disorders, Single-nucleotide polymorphism associated disease, Genetic diseases and disorders). ... The homozygous H63D variant is an indicator of the iron metabolism disorder hemochromatosis, which may increase the risk of ... 2010). "Prevalent Iron Metabolism Gene Variants Associated with Increased Brain Ferritin Iron in Healthy Older Men". J. ... Iron Disorders Institute nanograms. 2010. Nandar W, Connor JR (2011). "HFE Gene Variants Affect Iron in the Brain". J. Nutr. ...
... repair-deficiency disorders Glucose metabolism disorders Hyperlactatemia Iron metabolism disorders Lipid metabolism disorders ... The principal classes of metabolic disorders are: Acid-base imbalance Metabolic brain diseases Disorders of calcium metabolism ... Hur, Kyu Yeon; Lee, Myung-Shik (2015-06-01). "Gut Microbiota and Metabolic Disorders". Diabetes & Metabolism Journal. 39 (3): ... Metabolic disorder screening can be done in newborns via blood, skin, or hearing tests. Metabolic disorders can be treatable by ...
Bone marrow and hematopoietic stem cell transplantation Cellular disorders Chronic leukemias Disorders of iron metabolism ... Profiles Editorials Key Paper Evaluations Meeting Reports Clinical Trial Reports Acute leukemias Anemias Bleeding disorders ... failure syndromes Multiple myeloma and amyloidosis Neutropenia Non-Hodgkin lymphomas Pediatric hematology Platelet disorders ...
... there are no known genetic disorders of human iron metabolism that directly cause iron deficiency. Possible reasons that ... Mild iron deficiency can be prevented or corrected by eating iron-rich foods and by cooking in an iron skillet. Because iron is ... iron in meat (heme iron source) is more easily absorbed than iron in grains and vegetables ("non-heme" iron sources). Minerals ... Iron deficiency, or sideropenia, is the state in which a body lacks enough iron to supply its needs. Iron is present in all ...
Iron metabolism, Genetic diseases and disorders, Red blood cell disorders, Hepatology, Arthritis, Disturbances of human ... error of metabolism where this inherited disorder can increase the absorption of iron and thus cause tissue damage due to iron ... People with abnormal iron regulatory genes do not reduce their absorption of iron in response to increased iron levels in the ... Transferrin binds iron and is responsible for iron transport in the blood. Measuring ferritin provides a crude measure of iron ...
Iron metabolism, Autosomal recessive disorders, Congenital disorders, Rare diseases, Red blood cell disorders). ... Also, this excess iron deposits itself in the heart, liver and joints, and causes damage. Ferritin, the storage form of iron ... The missing protein without iron. Iron treatment is detrimental as it does not correct the anemia and is a cause of secondary ... The iron damage to the heart can lead to heart failure. The anemia is typically microcytic and hypochromic (the red blood cells ...
Hereditary haemochromatosis is a congenital disorder which affects the regulation of iron metabolism thus causing increased gut ... This protein mediates cellular uptake of transferrin-bound iron, and may be involved in iron metabolism, hepatocyte function ... Haemochromatosis type 3 is a type of iron overload disorder associated with deficiencies in transferrin receptor 2. It exhibits ... novel gene discovery and the molecular pathophysiology of iron metabolism". Human Molecular Genetics. 9 (16): 2377-2382. doi: ...
... iron metabolism, coenzyme A biosynthesis, phospholipid metabolism, ceramide metabolism, lysosomal disorders, as well as ... Central nervous system disorders, Extrapyramidal and movement disorders, Vitamin, coenzyme, and cofactor metabolism disorders) ... NBIA is not one disease but an entire group of disorders, characterized by an accumulation of brain iron, sometimes in the ... Phenotypes of the different disorders appear to be dependent on age, i.e. amount of iron accumulation and cognitive abilities. ...
Inborn errors of metal metabolism, Iron metabolism, Red blood cell disorders, Membrane transport protein disorders). ... African iron overload, also known as Bantu siderosis or dietary iron overload, is an iron overload disorder first observed ... Preparing beer in iron pots or drums results in high iron content. The iron content in home-brewed beer is around 46-82 mg/L, ... Iron reduction will likely require the removal of iron using specific drugs (iron-chelation). The physician may use a ...
Iron metabolism, Red blood cell disorders). ... Latent iron deficiency (LID), also called iron-deficient ... Total iron-binding capacity increases when iron deficiency exists. Serum ferritin levels reflect the iron stores available in ... Normal serum iron is between 60 and 170 micrograms per deciliter (μg/dL). Normal total iron-binding capacity for both sexes is ... Low levels (< 12 ng/mL) are specific for iron deficiency. However, inflammatory and neoplastic disorders can cause ferritin ...
For example, excess copper intake produces anemia by interfering with iron transport and/or metabolism. The identification of ... genetic disorders of copper metabolism leading to severe copper toxicity (i.e., Wilson disease) has spurred research into the ... Since copper availability in the body is hindered by an excess of iron and zinc intake, pregnant women prescribed iron ... Hart, E. B.; Steenbock, H.; Waddell, J. (1928). "Iron nutrition. VII: Copper is a supplement to iron for hemoglobin building in ...
... phospholipid metabolism problems have been seen in both this disorder and a related disorder called pantothenate kinase- ... also are associated with changes in brain iron metabolism. Researchers are studying the links between phospholipid defects, ... brain iron, and damage to nerve cells, but have not determined how the iron accumulation that occurs in some individuals with ... Autosomal recessive disorders, Pervasive developmental disorders, Rare diseases). ...
Early Work Minnich participated in early research into iron metabolism, including studies of fluctuation in women's iron levels ... Hemoglobin E While in Thailand in 1951, Minnich found an unusually high rate of thalassemias, blood disorders characterized by ... many centered around iron metabolism. She published over 45 scientific papers and 19 abstracts including noted work on blood ... Minnich found that that clay actually made iron deficiency worse by acting as a chelating agent, binding iron in the ...
Iron Metabolism, University of Virginia Pathology. Accessed 22 September 2007. Bridges, Kenneth R. "Transferrin and Iron ... Disorders of the proteins in these membranes are associated with many disorders, such as hereditary spherocytosis, hereditary ... Iron deficiency anemia is the most common anemia; it occurs when the dietary intake or absorption of iron is insufficient, and ... The iron is released into the plasma to be recirculated by a carrier protein called transferrin. Almost all red blood cells are ...
and requires iron and L-ascorbate as co-factors. Mutations in the TMLHE gene cause epsilon-trimethyllysine hydroxylase ... and autism spectrum disorders. TMLHE has been shown to have 14 binary protein-protein interactions including 12 co-complex ... deficiency (TMLHED), an inborn error of metabolism in carnitine biosynthesis, which may increase the risks of developing ... "Analysis of the chromosome X exome in patients with autism spectrum disorders identified novel candidate genes, including TMLHE ...
In thermodynamic terms, metabolism maintains order by creating disorder. As the environments of most organisms are constantly ... Dunn LL, Suryo Rahmanto Y, Richardson DR (February 2007). "Iron uptake and metabolism in the new millennium". Trends in Cell ... Metabolism Look up metabolism in Wiktionary, the free dictionary. Wikimedia Commons has media related to Metabolism. General ... The metabolism of cancer cells is also different from the metabolism of normal cells, and these differences can be used to find ...
... metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease-mineral and bone disorder ... "The iron-based phosphate binder PA21 has potent phosphate binding capacity and minimal iron release across a physiological pH ... Sucroferric oxyhydroxide, sold under the brand name Velphoro, is a non-calcium, iron-based phosphate binder used for the ... Sucroferric oxyhydroxide is also known as a mixture of polynuclear iron(III)-oxyhydroxide, sucrose and starches. The most ...
... can lead to: Obesity, a disorder which occurs by eating more calories than one burns, as well as: Oversupplying a ... For mineral excess, see: Iron poisoning, and Low sodium diet (a response to excess sodium). Overnutrition may also refer to ... The amount of nutrients exceeds the amount required for normal growth, development, and metabolism. ...
Human iron metabolism Iron deficiency anemia Roy CN, Andrews NC (October 2001). "Recent advances in disorders of iron ... Iron metabolism disorders may involve a number of genes including HFE and TFR2. Hepcidin is the master regulator of iron ... http://sickle.bwh.harvard.edu/menu_iron.html Andrews NC (December 1999). "Disorders of iron metabolism". N. Engl. J. Med. 341 ( ... So though many mysteries of iron metabolism remain, the discovery of hepcidin already allows a much better understanding of the ...
Disorders in the processing of iron in the body: its absorption, transport, storage, and utilization. (From Mosbys Medical, ...
Depletion of OTUD3 results in a disorder of iron metabolism. OTUD3 knockout mice display nigral iron accumulation, motor ... Iron regulatory protein 2 (IRP2) is a key factor in regulating brain iron homeostasis. Although two ubiquitin ligases that ... these findings demonstrate that OTUD3 is a bona fide deubiquitylase for IRP2 and plays a critical role in the nigral iron ... and stabilizes IRP2 protein in an iron-independent manner. ... 2: OTUD3 deletion induced disorder of iron metabolism.. a Iron ...
Impulsive behaviour is common in various neuropsychiatric disorders. Here, the authors identify a pathway from the lateral ... Behavioral impulsivity is common in various psychiatric and metabolic disorders. Here we identify a hypothalamus to ... Genome-wide analysis of a model-derived binge eating disorder phenotype identifies risk loci and implicates iron metabolism * ... affective disorders, attention-deficit hyperactivity disorder, and Parkinsons disease1. Recent attention has also implicated a ...
Iron Metabolism Disorders. *Irritable Bowel Syndrome. *Itchy Skin. *Joint Pain. *Knee Pain ...
Centre of Expertise for disorders of iron metabolism. Azienda Ospedaliera Universitaria Integrata di Verona - Ospedale Borgo ... Centre of Expertise for hemoglobinopathy and constitutional anemia due to iron metabolism disorders ... Centre of Expertise for rare anemias and congenital disorders of iron metabolism ... Centre of Expertise for rare anemias and congenital disorders of iron metabolism ...
Iron Metabolism Disorders. *Irritable Bowel Syndrome. *Itchy Skin. *Joint Pain. *Kidney Infection ...
Hemosiderosis caused by excessive iron intake (eg, multiple transfusions, excess iron administration) Acute iron poisoning ( ... Increases in serum iron level are associated with the following: Idiopathic hemochromatosis Liver necrosis (viral hepatitis) ... Beutler E. Disorders of Iron Metabolism. Prchal JT KK, Lichtman MA, Kipps TJ, Seligsohn U, ed. Williams Hematology. 8th ed. New ... Iron Study Interpretation. Increases in serum iron level are associated with the following [1, 2, 3, 4] :. * Idiopathic ...
Ginkgetin may provide neuroprotective therapy for Parkinsons disease and iron metabolism disorder related diseases.Dec 31, ... Diseases : Neurodegenerative Diseases, Neurologic Disorders. Pharmacological Actions : Iron Chelating Agents, Neuritogenic, ... Diseases : Iron Overload, Oxidative Stress. Pharmacological Actions : Anti-Apoptotic, Iron Chelating Agents, Neuroprotective ... Green tea catechins as brain-permeable, natural iron chelators-antioxidants for the treatment of neurodegenerative disorders. ...
Hyperferritinemia-cataract syndrome is a disorder characterized by an excess of an iron storage protein called ferritin in the ... Kato J, Niitsu Y. Recent advance in molecular iron metabolism: translational disorders of ferritin. Int J Hematol. 2002 Oct;76( ... Hyperferritinemia-cataract syndrome is a disorder characterized by an excess of an iron storage protein called ferritin. in the ... Ferritin stores and releases iron in cells. Each ferritin molecule can hold as many as 4,500 iron atoms inside its spherical ...
Iron Metabolism Disorders ... Alzheimers diseaseAnemiaArthritisAsthmaAutismBipolar disorder ... disordersHeart healthTransgender healthHepatitis CType 2 diabetesInflammationVaccinations and immunizationsLung cancerWeight ... disordersHeart healthTransgender healthHepatitis CType 2 diabetesInflammationVaccinations and immunizationsLung cancerWeight ... disordersStrokeTransgender healthType 1 diabetesType 2 diabetesUlcerative colitisVaccinations and immunizationsWeight ...
Categories: Iron Metabolism Disorders Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, ...
Other and unspecified disorders of iron metabolism. E83.111. Hemochromatosis due to repeated red blood cell transfusions. ... Blood contains a lot of iron. Because the body has no natural way to get rid of iron, the iron in transfused blood builds up in ... Yet, currently, there is no compelling evidence of the clinical effect of iron removal therapy on any neurological disorder. ... Aceruloplasminemia is a rare autosomal recessive disorder in which iron gradually accumulates in the retina, basal ganglia, and ...
Disorder of iron metabolism, unspecified [hyper-ferritinemic syndromes]. E83.19. Other disorders of iron metabolism [hyper- ... Cardiovascular Disorders. Heydari and associates (2021) stated that IL-1 is a pro-inflammatory cytokine that is produced by ... Other specified disorders of the skin and subcutaneous tissue [inflammatory] M04.9. Autoinflammatory syndrome, unspecified [Yao ... IL1β is known to be implicated in the development of chronic inflammatory disorders such as RA. These researchers examined the ...
Iron Metabolism Disorders ... Alzheimers diseaseAnemiaArthritisAsthmaAutismBipolar disorder ... disordersHeart healthTransgender healthHepatitis CType 2 diabetesInflammationVaccinations and immunizationsLung cancerWeight ... disordersHeart healthTransgender healthHepatitis CType 2 diabetesInflammationVaccinations and immunizationsLung cancerWeight ... disordersStrokeTransgender healthType 1 diabetesType 2 diabetesUlcerative colitisVaccinations and immunizationsWeight ...
Iron Deficiency Anemia * Iron Metabolism Disorders * Langerhans Cell Histiocytosis * Leukemia * Leukocytosis * Leukopenia ...
Iron Metabolism & its Disorders. Residual erythropoiesis protects against myocardial hemosiderosis in transfusion-dependent ... Platelet Biology & its Disorders. Bone marrow pathologic abnormalities in familial platelet disorder with propensity for ... Plasma Cell Disorders. Impact of prior therapy on the efficacy and safety of oral ixazomib-lenalidomide-dexamethasone vs. ... thalassemia by lowering labile plasma iron via transient generation of apotransferrin (641 Online Views) Maciej W. Garbowski, ...
This is the most common inherited liver disease in white persons and the most common autosomal recessive genetic disorder. ... Hemochromatosis is the abnormal accumulation of iron in parenchymal organs, leading to organ toxicity. ... Clinical consequences of new insights in the pathophysiology of disorders of iron and heme metabolism. Hematology Am Soc ... What is hemochromatosis? Hemochromatosis is a genetic disorder where the body isnt able to regulate its iron absorption. Iron ...
Iron Metabolism: Interactions with Normal and Disordered Erythropoiesis. Tomas Ganz and Elizabeta Nemeth. Erythroid Heme ... This book includes discussions of management and treatment strategies for hemoglobin disorders, such as transfusions, iron- ... The pathophysiological consequences of hemoglobin disorders (e.g., ineffective erythropoiesis and aberrant iron homeostasis), ... Hemoglobin and its Disorders: 150 Years of Study. David J. Weatherall, Alan N. Schechter, and David G. Nathan. Erythopoiesis: ...
Among the factors leading to pathological processes, microbes, viruses, gene dysregulation and immune system disorders have ... The treatment of black stain associated with of iron metabolism disorders with lactoferrin: A litterature search and two case ... Lactoferrin, as the name suggests (lacto + ferrin = milk + iron), is iron binding milk protein, which helps to balance iron ... Kazan, H.H.; Urfali-Mamatoglu, C.; Gunduz, U. Iron metabolism and drug resistance in cancer. BioMetals 2017, 30, 629-641. [ ...
Iron and Copper Deficiency and Disorder of Iron Metabolism *The Prophyrias and Prophyrinurias *Erythrocyte Enzyme Abnormalities ... Eosinophils and their Disorders *Basophils, Mast Cells and Their Disorders *Monocytes and Macrophages and Their Disorders * ... Structure, Function, and Disorders of Lymphoid Tissue *Disorders of the Spleen *Systemic Lupus Erythematosus *Feline ... Inherited Intrinsic Platelet Disorders *Acquired Platelet Dysfunction. Section VII. Hemostasis. *Overview of Hemostasis * ...
Inflammatory bowel disease, anaemia investigation, colorectal cancer, endoscopy, disorders of iron metabolism. ... Iron chelation: a potential therapeutic strategy in oesophageal cancer. Br J Pharmacol, 2013 Mar;168(6):1313-5. ... Is there a role for intravenous iron therapy in patients undergoing colorectal cancer resection? Expert Rev Anticancer Ther. ... Chris Tselepis 2# and Owen J Sansom 1# Luminal iron levels govern intestinal tumourigenesis following Apc loss in vivo. Cell ...
iron metabolism disorder causing increased iron storage.. *sickle cell anemia.. *anemia from pyruvate kinase and G6PD ... increased risk of bleeding due to clotting disorder.. How to treat macular edema in the eye?. Often, a non-steroidal anti- ...
This is the most common inherited liver disease in white persons and the most common autosomal recessive genetic disorder. ... Hemochromatosis is the abnormal accumulation of iron in parenchymal organs, leading to organ toxicity. ... Clinical consequences of new insights in the pathophysiology of disorders of iron and heme metabolism. Hematology Am Soc ... Hereditary hemochromatosis is an adult-onset disorder that represents an error of iron metabolism characterized by ...
The aim of this study was to detect the levels of 13 elements (Potassium (K), Sodium (Na), Calcium (Ca), Iron (Fe), Zinc (Zn), ... N. C. Andrews, "Disorders of iron metabolism," New England Journal of Medicine, vol. 341, no. 26, pp. 1986-1995, 1999. ... Elements such as Se, Cu, Mn, Fe, Ni, and Zn are essential for normal metabolism [6] but above tolerance limits they should be ... The aim of this study was to detect the levels of 13 elements (Potassium (K), Sodium (Na), Calcium (Ca), Iron (Fe), Zinc (Zn), ...
Hereditary hemochromatosis is a common inherited disorder of iron metabolism that leads to accumulation of iron in vital organs ... Iron. When people donate blood, their bodys iron levels also decrease. Eventually, low iron levels lead to low hemoglobin/ ... One laboratory test used to determine iron levels is called ferritin. A low ferritin result is a reliable indicator of iron ... Iron deficiency is common. Those who donate regularly or have heavier menstrual blood losses, recent pregnancy, or a meat-free ...
Disorders of iron and copper metabolism, the sideroblastic anemias, and lead toxicity. In: Orkin SH, Fisher DE, Ginsburg D, ... Serum iron Serum iron. A serum iron test measures how much iron is in your blood. ... Iron helps make red blood cells, so a lack of iron in the body may lead to anemia. The medical name of this problem is iron ... Total iron binding capacity. Total iron binding capacity (TIBC) is a blood test to see if you have too much or too little iron ...
2014). Sleep disorders: A review of the interface between restless legs syndrome and iron metabolism.. https://cdn.publisher. ... Iron. Doctors associate. low iron levels with RLS and other symptoms such as fatigue, depression, and thinking and reasoning ... Doctors classify RLS as a sleep disorder, as resting triggers the symptoms. They may also consider it a movement disorder, as ... Doctors have linked ADHD and RLS with reduced sleep quality and iron deficiency, believing that systemic iron deficiency ...
Iron homeostasis and disorders of iron metabolism. Molecular physiology and structure-function of human iron-transport proteins ... Fragile X syndrome; autism spectrum disorders.. [email protected]. Website. Esfandiari, Leyla. Dr. Esfandiari has a ... GTP energy metabolism; Signaling; Brain tumors; Brain metastatic cancers; Metabolic diseases; NAFLD; Biochemistry and cell ... Analysis of molecular mechanisms underlying brain disorders such as Fragile X syndrome, epilepsy and autism with the goal to ...
Disorders of iron metabolism: iron deficiency and overload. In: Hoffman R, Benz EJ Jr, Shattil SJ, Furie B, Cohen HJ, eds. ... Iron absorption by infants fed formula or milk. Spectrum of body iron content. Prevalence of iron deficiency and and iron- ... In iron-deficiency anemia, the most severe form of iron deficiency, the shortage of iron leads to underproduction of iron- ... Iron Metabolism Total body iron averages approximately 3.8 g in men and 2.3 g in women, which is equivalent to 50 mg/kg body ...
  • For instance, a severe form of iron overload, juvenile hemochromatosis, is a result of severe hepcidin deficiency. (wikipedia.org)
  • But the exact mechanisms of most of the various forms of adult hemochromatosis, which make up most of the genetic iron overload disorders, remain unsolved. (wikipedia.org)
  • Hereditary hemochromatosis when phlebotomy is not an option (e.g., poor candidate due to underlying medical disorders) or the member had an unsatisfactory response to phlebotomy. (aetna.com)
  • [ 64 ] Most patients are asymptomatic (75%) and are diagnosed when elevated serum iron levels are noted on a routine chemistry screening panel or when screening is performed because a relative is diagnosed with hemochromatosis. (medscape.com)
  • Cirrhosis is due to progressive iron deposition in the liver parenchyma, and it is one of the most common disease manifestations of the tissue damage caused by hemochromatosis. (medscape.com)
  • Hemochromatosis is the abnormal accumulation of iron in parenchymal organs, leading to organ toxicity. (medscape.com)
  • Once diagnosed, hemochromatosis is treated by phlebotomy to rid the body of excess iron and to maintain normal iron stores. (medscape.com)
  • Hereditary Hemochromatosis is a disorder characterized by iron deposition in several organs and hyperferritinemia. (scielo.br)
  • and diseases of iron metabolism, such as hemochromatosis. (utah.edu)
  • Before using this medication, tell your doctor or pharmacist your medical history, especially of: iron metabolism disorders (such as hemochromatosis), other types of anemia (such as pernicious anemia). (imedix.com)
  • The most common human disorder of iron overload is hereditary hemochromatosis, which leads to abnormal accumulation of iron in the liver, heart, skin, and other organs. (eurekalert.org)
  • Antidotes for iron toxicity are used in patients with hemochromatosis that is associated with significant anemia or severe end-organ involvement. (medscape.com)
  • Mechanisms of iron accumulation in hereditary hemochromatosis. (medscape.com)
  • Screening of patients with iron overload to identify hemochromatosis and porphyria cutanea tarda. (medscape.com)
  • Iron overload and hemochromatosis. (medscape.com)
  • Valenti L, Varenna M, Fracanzani AL, Rossi V, Fargion S, Sinigaglia L. Association between iron overload and osteoporosis in patients with hereditary hemochromatosis. (medscape.com)
  • Attenuated inflammatory responses in hemochromatosis reveal a role for iron in the regulation of macrophage cytokine translation. (medscape.com)
  • Mutations in HFE2 cause iron overload in chromosome 1q-linked juvenile hemochromatosis. (medscape.com)
  • Hemochromatosis (iron overload) is a typically systemic process in which iron deposition can cause tissue damage. (msdmanuals.com)
  • Спадковий гемохроматоз Hereditary hemochromatosis is a genetic disorder characterized by excessive iron (Fe) accumulation that results in tissue damage. (msdmanuals.com)
  • Hereditary HFE hemochromatosis accounts for most cases of excess body iron that result from increased iron absorption. (medscape.com)
  • [ 2 ] Homozygous C282Y hemochromatosis is the cause of 85%-90% of cases of iron overload. (medscape.com)
  • Other genetic mutations involved in iron homeostasis, which account for most of the remaining patients with inherited disorders of iron overload, include juvenile hemochromatosis (type 2), transferrin receptor 2 disease (type 3 hemochromatosis), and ferroportin disease (type 4 hemochromatosis). (medscape.com)
  • Type 1 hemochromatosis results from reduced hepcidin expression and increased iron absorption, exceeding the capacity of transferrin to transport iron. (medscape.com)
  • Human iron metabolism Iron deficiency anemia Roy CN, Andrews NC (October 2001). (wikipedia.org)
  • However, individuals with hyperferritinemia-cataract syndrome do not have an excess of iron, and with repeated blood draws will develop reduced iron levels leading to a low number of red blood cells ( anemia ). (medlineplus.gov)
  • Iron helps make red blood cells, so a lack of iron in the body may lead to anemia. (stlukes-stl.com)
  • The medical name of this problem is iron deficiency anemia. (stlukes-stl.com)
  • A diet that does not have enough iron is the most common cause of this type of anemia in children. (stlukes-stl.com)
  • If a healthy diet does not prevent or treat your child's low iron level and anemia, the doctor will likely recommend iron supplements for your child. (stlukes-stl.com)
  • In the past three decades, increased iron intake among infants has resulted in a decline in childhood iron-deficiency anemia in the United States. (cdc.gov)
  • As a consequence, the use of screening tests for anemia has become a less efficient means of detecting iron deficiency in some populations. (cdc.gov)
  • These recommendations update the 1989 'CDC Criteria for Anemia in Children and Childbearing-Aged Women' (MMWR 1989;38(22):400-4) and are the first comprehensive CDC recommendations to prevent and control iron deficiency. (cdc.gov)
  • CDC emphasizes sound iron nutrition for infants and young children, screening for anemia among women of childbearing age, and the importance of low-dose iron supplementation for pregnant women. (cdc.gov)
  • In the United States, the prevalence of iron-deficiency anemia among children declined during the 1970s in association with increased iron intake during infancy (1-3). (cdc.gov)
  • Because of this decline, the value of anemia as a predictor of iron deficiency has also declined, thus decreasing the effectiveness of routine anemia screening among children. (cdc.gov)
  • CDC requested the Institute of Medicine to convene an expert committee to develop recommendations for preventing, detecting, and treating iron-deficiency anemia among U.S. children and U.S. women of childbearing age. (cdc.gov)
  • There are high quality data that intravenous iron, compared to either oral iron or no iron, significantly decreases anemia and red blood cell (RBC) transfusion requirement in hospitalized patients, albeit with a potential increased risk of infection [ 6 ]. (biomedcentral.com)
  • Iron Heme Polypep-Folic Acid Tablet is a medication that combines iron, heme polypeptide, and folic acid to support red blood cell production, improve iron levels, and prevent or treat iron-deficiency anemia. (imedix.com)
  • It is used to treat or prevent iron deficiency anemia (low red blood cell count). (imedix.com)
  • SALT LAKE CITY - University of Utah School of Medicine researchers have developed a new tool that facilitates diagnosis of anemia related to chronic illness, as well as diseases of iron overload. (eurekalert.org)
  • An excess of hepcidin in the blood can result in anemia and a deficiency of hepcidin causes a build-up of iron that is damaging to body organs. (eurekalert.org)
  • Since both anemia and iron overload have various causes, it is often difficult to distinguish among those causes. (eurekalert.org)
  • Anemia is a deficiency of the oxygen-carrying molecules inside red blood cells which can be caused by iron deficiency, vitamin B12 or folate deficiency, or chronic illnesses. (eurekalert.org)
  • Iron profile, another tool to differentiate ACD from iron deficiency anemia (IDA), is both less expensive and less invasive. (paediatricaindonesiana.org)
  • The UIBC and TIBC are usually increased in patients with iron-deficiency anemia, in whom a transferrin saturation of 15% or less is noted. (medscape.com)
  • [ 1 , 7 ] A low serum iron concentration is typically present along with a normal transferrin saturation in individuals with anemia of chronic inflammation. (medscape.com)
  • The pathophysiological consequences of hemoglobin disorders (e.g., ineffective erythropoiesis and aberrant iron homeostasis), their clinical manifestations, and epidemiological trends are also described. (cshlpress.com)
  • Iron is required for erythropoiesis and is also essential for many other life-sustaining functions including deoxyribonucleic acid (DNA) and neurotransmitter synthesis, mitochondrial function and the innate immune response. (biomedcentral.com)
  • Intravenous iron therapies have largely been investigated in the context of erythropoiesis. (biomedcentral.com)
  • Вторинне перевантаження залізом Secondary iron overload results from excess absorption of iron, repeated blood transfusions, or excess oral intake, typically in patients with disorders of erythropoiesis. (msdmanuals.com)
  • Without genetic predisposition, secondary iron overload can develop in patients who have undergone multiple blood transfusions, those with ineffective erythropoiesis coupled with oral iron supplementation, or patients in end-stage liver disease. (medscape.com)
  • The mutations that cause hyperferritinemia-cataract syndrome are found in a segment of the gene called the iron responsive element (IRE). (medlineplus.gov)
  • Mutations in the IRE segment of the FTL gene prevent it from binding with IRP, interfering with the mechanism by which ferritin production is matched to iron levels and resulting in excess ferritin being formed. (medlineplus.gov)
  • Hereditary hyperferritinaemia-cataract syndrome (HHCS) is a rare disorder usually caused by heterozygous mutations in the iron-responsive element (IRE) in the 5' untranslated region (5'UTR) of the L-ferritin gene (FTL), disturbing the binding of iron regulatory proteins (IRPs) and the post-transcriptional regulation of ferritin expression. (nih.gov)
  • This assay can readily detect variations in hepcidin levels in the blood due to mutations in genes that are known to affect hepcidin levels, as well as mutations in other genes involved in iron metabolism. (eurekalert.org)
  • ABSTRACT A case-control study aimed to determine the prevalence of C282Y, H63D and S65C mutations of the HFE gene in -thalassaemia carriers and investigate their influence on iron absorption. (who.int)
  • The iron status in these subjects was studied and correlated with the HFE gene mutations. (who.int)
  • Notre étude a démontré que les mutations du gène HFE sont fréquentes en Égypte chez les porteurs d'une -thalassémie par rapport aux sujets témoins. (who.int)
  • The goal of therapy in patients with iron overload disorders is to remove the iron before it can produce irreversible parenchymal damage. (medscape.com)
  • The company's lead drug candidate, PTG-300, is a synthetic peptide that targets hepcidin, a protein that regulates iron metabolism, to treat iron overload disorders. (ashkon.com)
  • The ability to detect and measure hepcidin has important implications for the diagnosis of anemias and iron overload disorders related to hepcidin. (eurekalert.org)
  • Dr. Robert Adler, MD is an Endocrinology, Diabetes & Metabolism Specialist in Richmond, VA. They specialize in Endocrinology, Diabetes & Metabolism, has 53 years of experience, and is board certified in Diabetes, Metabolism & Endocrinology. (healthline.com)
  • Dr. Kruti Patel, MD is an Endocrinology, Diabetes & Metabolism Specialist in Great Neck, NY. (healthline.com)
  • They specialize in Endocrinology, Diabetes & Metabolism, has 11 years of experience, and is board certified in Diabetes, Metabolism & Endocrinology. (healthline.com)
  • This novel test would allow doctors to distinguish anemias and diseases of iron metabolism that arise from abnormalities in hepcidin from those that have other causes. (eurekalert.org)
  • This battery of measurements are used in the diagnosis and treatment of certain liver, heart, and kidney diseases, acid-base imbalance in the respiratory and metabolic systems, other diseases involving lipid metabolism and various endocrine disorders as well as other metabolic or nutritional disorders. (cdc.gov)
  • Symptomatic patients might have any of the characteristic manifestations of systemic iron overload: liver disease with the eventual development of cirrhosis and hepatocellular carcinoma, arthropathy, increased skin pigmentation, cardiomyopathy, diabetes mellitus, gonadal insufficiency and other endocrine disorders. (medscape.com)
  • Iron is an essential nutrient element required in cellular biosynthetic and metabolic processes [ 15 ]. (nature.com)
  • Behavioral impulsivity is common in various psychiatric and metabolic disorders. (nature.com)
  • His main research interests are metabolic and genetic liver diseases, with a special focus on non-alcoholic fatty liver disease and iron metabolism disorders. (eas-society.org)
  • Together with pH determination, bicarbonate measurements are used in the diagnosis and treatment of numerous potentially serious disorders associated with acid-base imbalance in the respiratory and metabolic systems. (cdc.gov)
  • Hyperferritinemia in iron metabolic syndromes (e.g. (bvsalud.org)
  • Birth defects can be defined as structural or functional abnormalities, including metabolic disorders, which are present from birth. (who.int)
  • This article describes the endocrine and metabolic disorders reported in patients with SCD, discusses their management, and identifies gaps in current knowledge and opportunities for future research. (medscape.com)
  • OTUD3 knockout mice display nigral iron accumulation, motor deficits, and nigrostriatal dopaminergic neurodegeneration, which resembles the pathology of PD. (nature.com)
  • Curcumin may represent a new horizon in managing iron overload-induced toxicity as well as in pathological diseases characterized by hepatic iron accumulation. (greenmedinfo.com)
  • Diabetes, often requiring insulin therapy, occurs due to progressive iron accumulation in the pancreas. (medscape.com)
  • Arthropathy is due to iron accumulation in joint tissues. (medscape.com)
  • Failure to maintain iron homeostasis early after a profound insult may result in an accumulation of highly reactive free iron, or non-transferrin bound iron, inflicting further oxidative stress on vulnerable organs or scavenged by invading microorganisms. (biomedcentral.com)
  • Morbidity is mainly due to iron accumulation in the endocrine organs (especially the pancreas, gonads, and pituitary), liver, and heart. (msdmanuals.com)
  • Progressive iron accumulation eventually overwhelms the body's capacity for safe sequestration of the excess. (medscape.com)
  • Hepcidin is the master regulator of iron metabolism and, therefore, most genetic forms of iron overload can be thought of as relative hepcidin deficiency in one way or another[1]. (wikipedia.org)
  • So, in people with ferroportin proteins that transport iron out of cells without responding to hepcidin's signals to stop, they have a deficiency in the action of hepcidin, if not in hepcidin itself. (wikipedia.org)
  • So though many mysteries of iron metabolism remain, the discovery of hepcidin already allows a much better understanding of the nature of iron regulation, and makes researchers optimistic that many more breakthroughs in this field are soon to come. (wikipedia.org)
  • These changes are mediated predominantly by the polypeptide hepcidin, which acts to decrease the absorption and availability of iron, despite acute phase increases in iron-binding proteins, such as ferritin, which may suggest normal or increased iron stores. (biomedcentral.com)
  • However, assays, including hepcidin, offer the potential to identify iron restriction despite the presence of inflammation and may be coupled with promising therapeutic options to address issues including nosocomial infection and functional recovery for patients admitted to the ICU. (biomedcentral.com)
  • The advent of safe and effective intravenous iron preparations provides an opportunity to explore the potential benefits of treating patients diagnosed with functional iron deficiency in the ICU, when enteral iron is ineffective due to the actions of hepcidin. (biomedcentral.com)
  • Iron balance in the body is regulated by the interaction between a liver-produced hormone called hepcidin and the iron transporting receptor ferroportin. (eurekalert.org)
  • Hepcidin binds to ferroportin resulting in decreased export of iron out of cells. (eurekalert.org)
  • Having an assay for hepcidin would make it much easier and it would also help in diagnosing iron overload diseases. (eurekalert.org)
  • Human hepcidin has both iron- and bacteria-related activities, while fish hepcidin genes evolved to separate these functions. (eurekalert.org)
  • Hepcidin, which is produced in the liver and to a smaller extent in adipocytes and macrophages, is a key regulator of iron absorption. (medscape.com)
  • [ 6 ] When iron levels are normal or elevated, hepcidin inhibits intestinal iron absorption. (medscape.com)
  • When iron levels are low (as in iron deficiency), hepcidin promotes iron absorption from the small intestine. (medscape.com)
  • [ 7 , 8 ] Hepcidin acts by binding to the iron exporter ferroportin, blocking the transport and release of iron, leading to retention of iron within enterocytes and reduced iron absorption. (medscape.com)
  • [ 9 ] Chronic ethanol ingestion also reduces hepcidin transcription, thereby increasing iron absorption. (medscape.com)
  • These genes represent multiple steps along the pathway of iron regulation, from the body's ability to sense iron, to the body's ability to regulate uptake and storage. (wikipedia.org)
  • Iron absorption is regulated based on the body's iron stores and is usually in balance with the body's needs. (msdmanuals.com)
  • Iodine is an essential component of the thyroid hormones involved you regulating the human body's metabolism. (cdc.gov)
  • Iron regulatory protein 2 (IRP2) is a key factor in regulating brain iron homeostasis. (nature.com)
  • Here, we report OTUD3 (OTU domain-containing protein 3) functions as a deubiquitylase for IRP2, interacts with IRP2 in the cytoplasm, de-polyubiquitylates, and stabilizes IRP2 protein in an iron-independent manner. (nature.com)
  • The IRE normally can attach (bind) to a protein called the iron regulatory protein (IRP). (medlineplus.gov)
  • Hemoglobin is an iron-containing protein in red blood cells that transports oxygen to tissues throughout the body. (cshlpress.com)
  • Ferritin is a protein inside your cells that stores iron. (stlukes-stl.com)
  • The thyroid hormone regulates energy and fat metabolism and protein synthesis by regulating different enzymes that are involved in those processes. (cdc.gov)
  • Almost two-thirds of the iron in the body (approximately 2.5 grams of iron) is found in hemoglobin, the protein in red blood cells that carries oxygen to tissues. (cdc.gov)
  • A serum iron test measures how much iron is in your blood. (stlukes-stl.com)
  • A measurement called iron saturation (serum iron/TIBC) often can show whether the child has enough iron in the body. (stlukes-stl.com)
  • Iron profiles included the measurements of serum iron (SI), total iron binding capacity (TIBC), transferrin saturation (TF), and serum ferritin (SF). (paediatricaindonesiana.org)
  • TIBC must not be confused with unsaturated binding capacity (UIBC), which represents the residual after subtraction of serum iron from TIBC. (medscape.com)
  • Historically, the possibility of iron deficiency was largely unexplored in critically ill patients due to the confounding effects of acute inflammation on commonly available iron measures, the lack of safe and effective treatments and uncertainty as to the clinical significance of deranged iron metabolism. (biomedcentral.com)
  • Iron deposits are neuropathological hallmark of Parkinson's disease (PD). (nature.com)
  • Parkinson's disease (PD) is one of the most common movement disorders characterized by decreased of dopaminergic neurons. (nature.com)
  • Cirrhosis reversibility after iron removal has been reported, usually early in the course of liver disease, although reversal of advanced liver disease with varices has also been reported. (medscape.com)
  • A combination of iron deposition and melanin causes the skin bronzing or hyperpigmentation that is typical of the disease. (medscape.com)
  • In clinical practice Professor Brookes has experience in all areas of Gastroenterology but has particular interests in anaemia, iron biology and endoscopy, and is the Inflammatory Bowel Disease lead at New Cross Hospital. (nuffieldhealth.com)
  • Orthotopic liver transplantation is the only therapeutic option when end-stage liver disease progresses despite iron-reduction therapy. (medscape.com)
  • Regenboog M, van Kuilenburg ABP, Verheij J, Swinkels DW and Hollak CEM (2016) Hyperferritinemia and iron metabolism in Gaucher disease: Potential pathophysiological implications. (scielo.br)
  • Protagonist Therapeutics Inc (PTGX) is a biopharmaceutical company focused on developing and commercializing peptide-based drugs to treat gastrointestinal and blood disorders, including inflammatory bowel disease, Crohn's disease, and beta-thalassemia. (ashkon.com)
  • The Gopal Laboratory studies mRNA transport, RNA metabolism and its regulation in healthy and diseased neurons, in order to identify therapeutic targets for neurodegenerative diseases such as Alzheimer's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. (yale.edu)
  • The pathogenesis of anaemia in cancer is multifactorial and includes classical features of the inflammatory anaemia of chronic disease, such as iron restriction within the reticuloendothelial system, an impaired biological activity of erythropoetin and a diminished proliferation of erythroid progenitor cells, all of which are the reflection of a cancer driven activated immune system ( 2 ). (iiarjournals.org)
  • Background and objective Non-anaemic iron deficiency (NAID) might alter the oxygen pathway in health and disease. (url.edu)
  • Iron and the anaemia of chronic disease: a review and strategic recommendations. (paediatricaindonesiana.org)
  • Iron overload in human disease. (msdmanuals.com)
  • Haemoglobinophathies (including thalassaemia and sickle cell disease) and glucose-6-phosphate dehydrogenase deficiency, which are not covered by the ICD10 definition of congenital anomalies account for 6% of all congenital disorders. (who.int)
  • The predicted risks of iron overload and endocrine organ failure increase with both the duration of disease requiring transfusion therapy and the number of transfusions. (medscape.com)
  • Disorders in the processing of iron in the body: its absorption, transport, storage, and utilization. (selfdecode.com)
  • Iron absorption and transport. (medscape.com)
  • Molecular aspects of iron absorption and HFE expression. (medscape.com)
  • Intestinal expression of genes involved in iron absorption in humans. (medscape.com)
  • This iron loss is balanced by absorption of a portion of the 10 to 20 mg of iron in a typical US diet. (msdmanuals.com)
  • Although the hyperferritinemia in this disorder does not usually cause any health problems other than cataracts, the elevated ferritin levels in the blood can be mistaken for a sign of certain liver disorders. (medlineplus.gov)
  • Working out the functions of each gene in this pathway will be an important tool for finding new methods of treating genetic disorders, as well as for understanding the basic workings of the pathway. (wikipedia.org)
  • In the Finberg Laboratory, we use genetic approaches to investigate mechanisms that regulate systemic iron balance in normal physiology and to understand how disruption of these mechanisms contributes to the pathogenesis of clinical disorders of iron metabolism. (yale.edu)
  • A genetic component is thought to contribute to the pathogenesis of African iron overload, but no gene has yet been identified. (msdmanuals.com)
  • Currently, sound estimates do not exist of the number of children who were born with a serious congenital disorder due to genetic or environmental causes. (who.int)
  • Endocrine dysfunction is the most common and earliest organ toxicity seen in subjects with chronic iron-induced cellular oxidative damage and can be seen in those without clinical evidence of iron overload. (medscape.com)
  • [ 4 ] H63D mutation does not result in constitutional iron overload unless it occurs as a compound heterozygote with C282Y (C282Y/H63D). (medscape.com)
  • Ferritin stores and releases iron in cells. (medlineplus.gov)
  • Each ferritin molecule can hold as many as 4,500 iron atoms inside its spherical structure. (medlineplus.gov)
  • This storage capacity allows ferritin to regulate the amount of iron in cells and tissues. (medlineplus.gov)
  • This normally occurs when iron levels are low, because under those circumstances less ferritin is needed to store the iron. (medlineplus.gov)
  • The associated inflammatory response involves an increase in serum ferritin levels, which provides a defense against the growth of microorganisms by limiting the availability of circulating iron ( Cherayil, 2011 Cherayil BJ (2011) The role of iron in the immune response to bacterial infection. (scielo.br)
  • Here, the proband of a consanguineous family displayed moderate bilateral cataracts and elevated serum ferritin in the absence of iron overload. (nih.gov)
  • This study used a quasi-experimental design to compare the effectiveness of the CDS tool, which consisted of a best-practice alert (BPA) and provider education, in increasing the number of ferritin test orders to assess transfusional iron overload in adults with SCD. (cdc.gov)
  • Evaluation of serum ferritin in screening for iron deficiency in tuberculosis. (paediatricaindonesiana.org)
  • Assessing the state of iron-overload in patients with SCD constitutes a diagnostic challenge because of the unreliability of serum ferritin levels and the risks associated with liver biopsy. (medscape.com)
  • [5] Iron overload results primarily in an increase in storage iron held in ferritin and hemosiderin. (medscape.com)
  • Under various iron conditions, IRPs could bind to IREs in the targeted mRNA, stabilize the mRNA or prevent its translation. (nature.com)
  • Congenital disorders are a common condition. (who.int)
  • The most common serious congenital disorders are congenital heart defects, neural tube defects and Down syndrome. (who.int)
  • Considerable uncertainties remain as to the incidence and mortality due to congenital disorders, especially in countries which lack adequate registration of deaths. (who.int)
  • Our mission is to provide innovative and cutting-edge patient care for those with blood disorders, conduct basic, translational, and clinical research, train the next generation of hematologists, and promote faculty and staff well-being, diversity, and inclusion. (utah.edu)
  • In summary, the available evidence suggests that both iron deficiency and iron excess may be harmful for critically ill patients and that clinical assessment of iron status in the ICU is important and should include consideration of both possibilities. (biomedcentral.com)
  • The purpose of this study was to evaluate the effectiveness of a clinical decision support (CDS)-based intervention system for transfusional iron overload in adults with SCD to improve management in primary care. (cdc.gov)
  • An electronic medical record based clinical decision support system for potential transfusional iron overload in SCD patients in primary care was evaluated. (cdc.gov)
  • Transfusional iron overload is a significant clinical issue in patients with SCD. (cdc.gov)
  • is focal deposition of iron that typically does not cause tissue damage. (msdmanuals.com)
  • This book includes discussions of management and treatment strategies for hemoglobin disorders, such as transfusions, iron-chelating agents, gene therapy, and stem cell transplantation. (cshlpress.com)
  • Red blood cell transfusions are a therapeutic mainstay in SCD and repeated transfusions can result in iron overload. (medscape.com)
  • Repeated transfusions are associated with iron overload and possible iron-induced organ damage. (medscape.com)
  • In the Braddock Laboratory, we study the pathophysiology of benign and malignant hematologic disorders using biochemical and biophysical methods. (yale.edu)
  • Each day the body absorbs approximately 1-2 mg of iron to compensate for the 1-2 mg of iron that the (nonmenstruating) body loses (Institute of Medicine 2001). (cdc.gov)
  • HH is classified as an autosomal recessive disorder, with mostly European ancestry. (scielo.br)
  • We also study neurological disorders such as creatine deficiency syndromes. (uc.edu)
  • Curcumin supplementation would be effective in alleviating iron overload in patients with β-thalassemia intermedia. (greenmedinfo.com)
  • Effect of iron supplementation on mild to moderate anaemia in pulmonary tuberculosis. (paediatricaindonesiana.org)
  • Doctors have linked ADHD and RLS with reduced sleep quality and iron deficiency, believing that systemic iron deficiency contributes to around 43% of RLS-associated conditions. (medicalnewstoday.com)
  • 4 Iron metabolism: regulation and diseases group, Josep Carreras Leukaemia Research Institute (IJC), Campus ICO - Germans Trias i Pujol, Badalona, Spain. (nih.gov)
  • Too little iron can interfere with these vital functions and lead to morbidity and mortality. (cdc.gov)
  • High serum transferrin saturation and iron concentration are independent predictors of mortality in patients admitted to the ICU [ 2 ]. (biomedcentral.com)
  • Elevated iron has been shown to have a detrimental effect on mortality as well as quality of life. (cdc.gov)
  • http://sickle.bwh.harvard.edu/menu_iron.html Andrews NC (December 1999). (wikipedia.org)
  • Depletion of OTUD3 results in a disorder of iron metabolism. (nature.com)
  • In the majority patients, the insulin requirements or glucose level was not influenced by iron depletion. (medscape.com)
  • Chelation therapy with deferoxamine-induced iron depletion is administered in people with C282Y homozygosity unable to undergo phlebotomy. (medscape.com)
  • If humans do not get enough iodine, they can develop these disorders:Did you know that Iodine deficiency is the most preventable cause of mental retardation in the world (World Health Organization 2007)? (cdc.gov)
  • Total iron binding capacity (TIBC) is a blood test to see if you have too much or too little iron in your blood. (stlukes-stl.com)
  • Both iron and TIBC were assessed -thalassaemia trait alone does Sample usingstandardcolorimetrickitsbyau- notleadtoironoverload,andsome tomatedanalyser(BeckmanCoulter genemodifiersandacquiredcausesare Thisstudywascarriedoutduringthe SynchronCX9Pro).Normalrangefor reportedtomodulatetheexpression periodbetweenMarchandDecember ironwas70-200µg/dLandforTIBC ofhereditaryhaemochromatosis[6]. (who.int)
  • The sum of the UIBC and the plasma iron is the total iron-binding capacity (TIBC). (medscape.com)
  • Total iron-binding capacity (TIBC) is an indirect method assessment of transferrin levels. (medscape.com)
  • The relationship of TIBC and transferrin is disrupted in individuals with conditions that affect transferrin-binding capacity or other iron-binding proteins. (medscape.com)
  • Attention deficit hyperactivity disorder (ADHD) and restless legs syndrome (RLS) may have a correlation. (medicalnewstoday.com)
  • Combined iron-chelation and silymarin therapy was effective for improving the iron-burden status in patients with β-thalassemia major. (greenmedinfo.com)
  • Therapeutic potential of silymarin as a natural iron-chelating agent in β-thalassemia intermedia. (greenmedinfo.com)
  • Iron deficiency is the most common known form of nutritional deficiency. (cdc.gov)
  • Despite its importance in maintaining health, iron deficiency is the most common nutritional deficiency worldwide and many of the risk factors for iron deficiency are also risk factors for developing critical illness. (biomedcentral.com)
  • These conditions result in excess iron in the body and may be treated by blood-drawing. (medlineplus.gov)
  • The measurement of the blood's capacity to bind iron with transferrin is the iron-binding capacity. (medscape.com)
  • [ 1 ] Direct measurement of total iron-binding capacity may also be performed. (medscape.com)
  • Intracellular iron levels are elaborately balanced by iron efflux, uptake, and storage proteins that are regulated by iron regulatory proteins (IRPs, including IRP1 and IRP2) [ 16 ]. (nature.com)
  • Iron functions as a component of proteins and enzymes. (cdc.gov)
  • Exceptions to this rule detract considerably from the diagnostic value of measuring transferrin saturation in patients with suspected iron deficiency. (medscape.com)
  • which means one copy of the altered gene in each cell is sufficient to cause the disorder. (medlineplus.gov)
  • Among the factors leading to pathological processes, microbes, viruses, gene dysregulation and immune system disorders have been described. (mdpi.com)
  • Birth defects are a diverse group of disorders of prenatal origin which can be caused by single gene defects, chromosomal disorders, multifactorial inheritance, environmental teratogens and micronutrient deficiencies. (who.int)