Abstract
Although iron is an essential trace element for energy production and synthesis of red cells, excess iron causes cell damage because the living body lacks a pathway for passive iron elimination. Iron accumulates in animal tissue as a result of aging. Hepcidin-25 is a peptide hormone that negatively controls iron metabolism through suppression of iron secretion from reticuloendothelial macrophages and iron absorption from the intestine. Our present investigation of the relationship between serum hepcidin-25 and age-related iron accumulation revealed that the level of hepcidin-25 increased with aging. It was suggested that induction of hepcidin-25 led to accumulation of iron in reticuloendothelial macrophages and suppressed the absorption of iron from the intestine through reduced production of red cells and a reduction in the growth rate. In addition, iron accumulation was further increased due to suppression of iron secretion from reticuloendothelial macrophages by hepcidin-25. Further nutritional investigations are needed to clarify the need for iron and the chemical state of iron for absorption in non-bleeding mature and aged animals.
