Hepcidin treatment in Hfe−/− mice diminishes plasma iron without affecting erythropoiesis.

Eur J Clin Invest 2010; 40 (6): 511–517 Background Iron is essential for mammalian metabolism and its cellular concentration is controlled by regulating its acquisition and storage. Haemochromatosis is a condition involving iron overload that is characterised by increased duodenal iron absorption and a progressive accumulation of iron in vital organs. Hepcidin is the main hormone that regulates iron homoestasis and it is secreted by the liver. Materials and methods We have studied how extended hepcidin administration affects the iron load status, plasma and tissue iron concentration, erythropoiesis and the expression of proteins involved on iron homeostasis in haemochromatotic ( Hfe −/− ) and wild-type mice. Results Hepcidin reverted the high plasma iron concentrations in Hfe −/− mice to normal values. The high concentration of hepatic iron was not altered in the liver of these Hfe −/− mice. Hepcidin administration did not disturb erythropoiesis in either Hfe −/− or wild-type mice and likewise, hepcidin did not modify the expression of any protein analysed in the liver, duodenum or spleen of Hfe −/− and wild-type mice. These data confirm that hepcidin administration diminishes plasma iron concentrations. Conclusion Treatment with sustained doses of hepcidin diminishes plasma iron concentrations in Hfe −/− mice. [ABSTRACT FROM AUTHOR]