Normal iron metabolism is highly regulated and takes a crucial role in the maintenance of cell functions. The plasmatic iron bioavailability control is a key step of this metabolism which involves numerous proteins implicated at various levels, including the digestive iron absorption by enterocytes, and iron release from macrophages. These two phenomenons are modulated in a coordonated fashion by the plasmatic level of hepcidin, a peptide mainly synthetized by the liver, secreted in plasma and modulating the expression of ferroportin, the cellular exporter of iron, and thus the iron egress. Numerous factors are able to modulate the hepcidin expression, including iron status, erythropoietic activity, inflammation and hepatic status which are already identified. Abnormalities occurring in the regulation of hepcidin expression may favour the development of iron metabolism disturbance, including systemic iron overload or relative iron deficiency. The use of hepcidin for diagnostic purpose or as a therapeutic target remains to be determined.