Abstract
Previously, we have reported that rats with protein-energy malnutrition suffer from impaired iron metabolism due to induction of hepcidin-25. Supply of iron under conditions of high levels of hepcidin-25 would carry a risk of iron overload. In this study, hepcidin-25 kinetics and iron metabolism were investigated after protein re-feeding in rats with protein-energy malnutrition. Iron metabolism under conditions of iron supply was also investigated. Supply of protein in the protein re-feeding period allowed an increase of hepcidin-25 in serum, followed by a temporary reduction, and enhancement of iron deposition in the spleen. On the other hand, when no iron was supplied, iron deficiency anemia occurred, but slight iron deposition in the spleen was still observed. These results suggest that in protein-energy malnutrition, impairment of iron utilization may persist even after protein re-feeding once the protein has accumulated.
