Iron deficiency is a major public health problem and the most common nutritional cause of anemia. However, most genetic
A general model for the regulation of intestinal iron absorption is depicted. Although this model is still somewhat speculative, recent data suggest that the four known regulators (iron stores, erythropoietic demand, hypoxia and inflammation) may all act by modulating hepatic production of hepcidin, an iron-regulatory hormone. Increased iron stores and inflammation both appear to increase hepcidin expression (-►), whereas increased erythropoietic demand and hypoxia appear to decrease hepcidin expression (±).
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