Regulation of Iron Equilibrium

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Regulation of Iron Equilibrium

Regulation of iron equilibrium occurs mainly through the process of absorption. Iron is absorbed through the mucosal cells lining the duodenum. A variety of proteins are involved in this process. Hepcidin, an antimicrobial protein primarily produced in the liver, has recently been found to be a significant (negative) regulator of dietary iron absorption by disrupting cellular iron transport in the intestine. Decreased levels of hepcidin are related to increased iron absorption into the bloodstream. Hepcidin is increased in response to iron overload and inflammation.5
Additional proteins involved in iron metabolism include transferrin (Tf), transferrin receptor (TfR), ferroportin, HFE protein, hemojuvelin, and others. Their roles in iron absorption are complex and, in some instances, not completely understood.
Factors affecting iron absorption include:
  • Tissue stores
    • Decreased stored iron is associated with a decrease in hepcidin and an increase in iron absorption.
  • Rate of hematopoietic activity
    • An increased rate of erythropoiesis is associated with a decrease in hepcidin and an increase in iron absorption.
    • Oxygen concentration in tissues
      • Hypoxia decreases hepcidin and increases iron absorption, thereby promoting increased erythropoiesis.
      • Dietary intake, including a form of iron ingested
          • Heme iron is more readily absorbed than non-heme forms of iron.
            • Condition of GI tract mucosal cells
            • Intraluminal factors
              • Intestinal motility