Search results
Results from the WOW.Com Content Network
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.
Elevated serum ferritin, an indicator of blood iron levels, and transferrin saturation, which is involved with absorption of iron from the gut, are very common. [2] [3] Transferrin saturation may approach or reach 100%, where a normal value would lie between 16% and 45%. If transferrin saturation is normal, juvenile hemochromatosis can be ruled ...
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.
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.
The same can occur with elements in food, such as calcium, which impacts both heme and non-heme iron absorption. [39] Absorption of iron is better at a low pH (i.e. an acidic environment), and absorption is decreased if there is a simultaneous intake of antacids. Many other substances decrease the rate of non-heme iron absorption.
The most common type is iron-deficiency anemia, in which a lack of iron leads to a reduction in the number of red blood cells or hemoglobin. This can impair oxygen transport throughout the body.
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] .
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]