An iron exporter of iron highly expressed in absorptive duodenal enterocytes and in liver tissue macrophages.
A transmembrane iron exporter that transfers iron out of cells.
Allows dietary iron taking from absorptive cells to enter the circulation, and allows macrophages that recycle used ion from effete red cells.
Sole cellular iron exporter found on the basolateral surface of duodenal enterocytes and on macrophages and hepatocytes.
Ferroportin has a key role in increasing the bioavailability of iron.
Mutations in type hemochromatosis induces predominant macrophage iron overload.
Is the molecular target of hepcidin which is the major regulator of intestinal iron absorption and iron recycling from macrophages.
Hepcidin is a small peptide reduced by the liver, controls the activity of ferroportin by attaching to it and targeting proteins for destruction in the lysozyme.
Hepcidin levels fluctuate in response to the body’s need for iron causing less iron absorption with elevated levels, and lower levels of hepcidin associated with more iron absorption.
Its absence on cell surface leads to reduced iron efflux from macrophages and hepatocytes and decreased dietary iron absorption in the enterocytes.
When plasma levels of iron are low the synthesis of hepcidin is down regulated leading to increased ferroportin expression on cell surface and increased dietary iron absorption and iron efflux from the macrophages.