Fig. 3.

Regulating iron absorption by hepcidin-dependent and independent mechanisms. At the duodenal enterocyte, where iron is absorbed, hepcidin functions as a negative regulator at the basolateral surface, where ferroportin exports iron from duodenal enterocytes into the circulation. Hypoxia functions as a positive regulator at the apical surface where DMTI imports iron into duodenal enterocytes. Together, the presence of hypoxia in the gastrointestinal tract with suppression of hepcidin would provide the most potent stimulus for iron absorption. In PV, it is thus possible that, despite hepcidin suppression, hypoxia is diminished by erythrocytosis, preventing recovery from iron deficiency. DMTI divalent metal transporter 1, FPN ferroportin, PV polycythemia vera