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Hepcidin is a peptide hormone produced in the liver that plays a crucial role in iron homeostasis. Iron is an essential part of oxygen transport within the body and is present in hemoglobin, myoglobin, and the electron transport chain. Serum iron levels must be tightly regulated to ensure an adequate supply is available for hemoglobin synthesis during erythropoiesis, without allowing iron overload to occur in the body. Hepcidin decreases the level of iron by reducing dietary absorption and inhibiting iron release from cellular storage. Hepcidin production increases when iron levels rise above the normal range of 65 to 175 mcg/dL in males and 50 to 170 mcg/dL in females.
Hepcidin is an acute-phase reactant, one of many molecules whose plasma concentration changes in response to inflammation. During states of acute or chronic inflammation, levels of hepcidin and other acute-phase reactants increase, leading to a decrease in serum iron levels as hepcidin levels rise. Increased hepcidin correlates with the pathophysiology of anemia of chronic disease; the increase in inflammation causes a reduction in serum iron levels because the increase in hepcidin reduces iron transport out of cells. Conversely, a deficiency in hepcidin production can result in iron overload, as seen in hereditary hemochromatosis.
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