Submitted June 13, 2006
Accepted July 11, 2006
Suppression of hepcidin during anemia requires erythropoietic activity
Mihwa Pak, Miguel A Lopez, Victroia Gabayan, Tomas Ganz, and Seth Rivera*
David Geffen School of Medicine at the University of California, Los Angeles
* Corresponding author; email: sethrivera{at}mednet.ucla.edu.
Hepcidin, the principal iron regulatory hormone, regulates the absorption of iron from the diet and the mobilization of iron from stores. Previous studies indicated that hepcidin is suppressed during anemia, a response that would appropriately increase the absorption of iron and its release from stores. Indeed, in the mouse model, hepcidin-1 was suppressed after phlebotomy or erythropoietin administration but the suppression was reversed by inhibitors of erythropoiesis. The suppression of hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoiesis and is not directly mediated by anemia, tissue hypoxia or erythropoietin.
