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The body regulates iron levels by regulating each of these steps. For instance, enterocytes synthesize more Dcytb, DMT1 and ferroportin in response to iron deficiency anemia. [13] Iron absorption from diet is enhanced in the presence of vitamin C and diminished by excess calcium, zinc, or manganese. [14]
Absorption of dietary iron in iron salt form (as in most supplements) varies somewhat according to the body's need for iron, and is usually between 10% and 20% of iron intake. Absorption of iron from animal products, and some plant products, is in the form of heme iron, and is more efficient, allowing absorption of from 15% to 35% of intake.
Duodenal cytochrome B (Dcytb) also known as cytochrome b reductase 1 is an enzyme that in humans is encoded by the CYBRD1 gene.. Dcytb CYBRD1 was first identified as a ferric reductase enzyme which catalyzes the reduction of Fe 3+ to Fe 2+ required for dietary iron absorption in the duodenum of mammals. [5]
The iron in cytochromes usually exists in a ferrous (Fe 2+) and a ferric (Fe 3+) state with a ferroxo (Fe 4+) state found in catalytic intermediates. [1] Cytochromes are, thus, capable of performing electron transfer reactions and catalysis by reduction or oxidation of their heme iron. The cellular location of cytochromes depends on their function.
The process of iron transportation consists of iron being reduced by ferrireductases that are present on the cell surface or by dietary reductants such as ascorbate . [10] Once the Fe 3+ has been reduced to Fe 2+ , the DMT1 transporter protein transports the Fe 2+ ions into the cells that line the small intestine ( enterocytes ). [ 10 ]
Hepcidin is a protein that in humans is encoded by the HAMP gene. Hepcidin is a key regulator of the entry of iron into the circulation in mammals. [6]During conditions in which the hepcidin level is abnormally high, such as inflammation, serum iron falls due to iron trapping within macrophages and liver cells and decreased gut iron absorption.
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The liver produces hepcidin. Hepcidin controls iron absorption in the gastrointestinal tract and iron release from reticuloendothelial tissue. Iron must be released from macrophages in the bone marrow to be incorporated into the heme group of hemoglobin in erythrocytes. There are colony forming units that the cells follow during their formation.