hepcidin


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A 25-residue peptide hormone encoded by the HAMP gene, produced by the liver, and now regarded as the master regulator of iron homeostasis in humans and other mammals. Hepcidin is a direct inhibitor of ferroportin, a protein present in enterocytes and macrophages, which transports iron out of cells and into storage pools

hepcidin

(hĕp′sĭd-ĭn)
A protein secreted by the liver that acts as a regulatory hormone that controls the amount of iron in the body. Elevated levels of hepcidin in the blood prevent iron from being taken up by red blood cells. Hepcidin levels rise in many chronic illnesses and infections, causing the anemia of chronic disease. Proteins that block the action of hepcidin result, by contrast, in iron overload diseases such as hemochromatosis.
References in periodicals archive ?
Iron biology, immunology, aging, and obesity: four fields connected by the small peptide hormone hepcidin.
Hepcidin deficiency causes hereditary hemochromatosis, characterized by body iron overload that may progress to liver cirrhosis.
11) A recent study conducted on 12 physically active women (aged 19 to 32 years) found that hepcidin was increased 3 hours after either a 60-minute or 120-minute run at 65% of maximal oxygen uptake (V[O.
Drug Profiles discussed in this report include ACY-957, ALN-TMP, Antisense Oligonucleotides to Inhibit BCL11A and KLF1 for Hematological Disorders, BB-305, BtX-13, CNTO-530, Gene Therapy for Sickle Cell Disease and Beta Thalassemia, Gene Therapy for Sickle Cell Disease and Thalassemia, glutamine, luspatercept, NiCord, PB-04, Peptide Agonists of Hepcidin for Beta-Thalassemia and Juvenile Hemochromatosis, Project x-1450, ruxolitinib phosphate, Small Molecule to Inhibit Histone Deacetylase for Beta-Thalassemi, sotatercept, Stem Cell Therapy for Beta Thalassemia, Synthetic Peptides Hematological and Genetic Disorders, Thalagen.
Hepcidin controls iron levels by interacting directly with FPN1 in duodenal enterocytes, hepatocytes, and macrophages resulting in internalization and degradation of FPN1 (Nemeth, 2005)".
1) However, Stack and colleagues (11) observed that both high %TS values (reflecting increased iron plus redox-active iron) and low %TS values, likely a result of high hepcidin concentrations rather than reduced iron concentrations per se (12), are associated with increased total and cardiovascular mortality.
The identification of hepcidin has enabled a better understanding of the relationship between iron homeostasis and anemia of chronic disease.
Hemoglobin, Ferritin, Transferrin, and Hepcidin are major molecules which are critical in the function and regulation of iron.
Since hepcidin inhibits iron exportation from cells by blocking ferroportin activity, the root cause of the hypoferremia and iron-restricted erythropoiesis in ACD can be attributed to the excess hepcidin levels.
The liver produces hepcidin, a hormone that inhibits iron from being absorbed in the gut and also prevents it from getting into the bloodstream.