Minihepcidin Treatment Prevents Hemochromatosis Phenotype in Hepcidin Knockout Mice. In hereditary hemochromatosis, because of hepcidin deficiency, iron is excessively exported into plasma, both from enterocytes, which absorb dietary iron and from macrophages, which recycle iron from old red blood cells. This process results in iron overload of hepatocytes in the liver and iron-deficient spleen macrophages, as shown in the top row of the figure for knockout mice treated with solvent only. In the bottom row, two weeks of daily minihepcidin injections prevented liver iron accumulation and caused normalization of iron stores in spleen macrophages.