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The absorption of dietary iron is a variable and dynamic process. The amount of iron absorbed compared to the amount ingested is typically low, but may range from 5% to as much as 35% depending on circumstances and type of iron. The efficiency with which iron is absorbed varies depending on the source.
The absorption of dietary iron is a variable and dynamic process. The amount of iron absorbed compared to the amount ingested is typically low, but may range from 5% to as much as 35% depending on circumstances and type of iron. The efficiency with which iron is absorbed varies depending on the source.
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.
The most significant factor regulating iron uptake is the amount of iron present in the body. Iron absorption increases with sufficient iron storage and vice versa. Increased erythrocyte synthesis also stimulates iron absorption in the gut. [15] Therefore, oral bioavailability of iron varies greatly, ranging from less than 1% to greater than 50 ...
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 ]
Iron deficiency, or sideropenia, is the state in which a body lacks enough iron to supply its needs. Iron is present in all cells in the human body and has several vital functions, such as carrying oxygen to the tissues from the lungs as a key component of the hemoglobin protein, acting as a transport medium for electrons within the cells in the form of cytochromes, and facilitating oxygen ...
Hypochromic anemia may be caused by vitamin B6 deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections (e.g. hookworms) or other diseases (i.e. anemia of chronic disease), therapeutic drugs, copper toxicity, and lead poisoning.
Iron metabolism disorders may involve a number of genes including HFE and TFR2. [ 1 ] 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] .
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