Iron excess increases the hepatic expression of hepcidin, the systemic iron metabolism regulator, that favors the iron sequestration in the spleen. Genetic iron overload related to hepcidin insufficiency decreases the spleen iron concentration, and increases hepatic iron concentrations, hereas during secondary iron overload the hepcidin expression increases together with spleen iron concentration, in addition to hepatic iron concentrations increase. Links between iron metabolism and other metals being suggested, our aim was to investigate, during iron overload, the relationships between the hepatic hepcidin expression level and the hepatic and splenic concentrations of iron, manganese, copper, zinc and molybdenum, determined using ICP-MS. Hepcidin-deficient mice, secondary iron overload mice models and their respective controls were studied. Spleen molybdenum and manganese concentrations paralleled the modulation of: i) spleen iron concentrations, increasing in secondary iron overload, and decreasing in hepcidin deficiency related iron overload, ii) hepatic hepcidin mRNA expression. Our data suggest that iron, manganese and molybdenum metabolisms could share mechanisms controlling their distribution that are associated to hepcidin modulation. In diseases with abnormal hepcidin levels, including chronic inflammation, special attention should be paid to those metals that could participate to the phenotype.