A newly identified iron regulator, hepcidin, appears to communicate body iron status and demand for erythropoiesis to the intestine, and in turn, modulates intestinal iron absorption. Hepcidin was first purified from human blood and urine as an antimicrobial peptide and was found to be predominantly expressed in the liver. A lack of hepcidin expression has been associated with iron overload and overexpression of hepcidin results in iron-deficiency anemia in mice. In addition, hepcidin levels decrease in mice fed a low iron diet and increase in mice fed a high iron diet. These observations support the role of hepcidin as a signal that limits intestinal iron absorption. Hepcidin expression is also affected by hypoxia and inflammation and is decreased in hemochromatosis patients. Thus, the relationship between body iron status and hepcidin is altered in hemochromatosis patients. In addition, hepcidin is decreased in HFE knockout mice, which demonstrates characteristics of iron overload as in hemochromatosis patients. Hence, HFE is suggested to act as a regulator of hepcidin expression. Transcription factors, such as C/EBPalpha, are also suggested to be involved in the regulation of hepcidin gene expression. However, much remains to be investigated in the regulation of hepcidin by iron, hypoxia and inflammation.