Homocysteine as a cause of ischemic heart disease: the door remains open.

as an important regulator of several liver functions. In the hepatic response to fasting, PGC-1 has been shown to coordinate the induction of gluconeogenic enzymes by coactivating such liver-enriched transcription factors as hepatocyte nuclear factor 4 (HNF4 ) and forkhead box O1 protein (FOXO1), as well as the glucocorticoid receptor (3). Whether these regulators are involved in the control of hepcidin gene expression by fasting awaits further investigations. Ourresultssuggestthatactivation of the expression of the gene encoding hepcidin during fasting could be due not only to systemic regulation (such as decreased erythropoiesis, as suggested by Troutt et al.) but also to PGC-1 – dependent cell autonomous activation. This increase of hepcidin1 by fasting can explain the results of Conrad et al. (4 ), who were the first to show that 5 days of starvation in rats led to decreased absorption of iron administered orally. This observed increase in hepcidin with fasting also is in agreement with the recent report by Papillard-Marechal et al. (5), who found increased serum hepcidin concentrations in patients with anorexia nervosa, the increased hepcidin concentrations in their study being independent of inflammation and iron overload.