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Recently discovered peptide-hepcidin (Hepc) may be a central player in the communication of iron body stores to the intestinal absorptive cells and thus involved in the maintenance of iron homeostasis. The aim of this study was to determine the effects of the level of dietary iron on Hepc gene expression in the liver. OF1 male mice were fed for 3 weeks either control diet (35 mg iron/kg diet), low-iron diet (1 mg iron/kg diet), or high-iron diet (500 mg iron/kg diet), and Hepc 1 and 2 mRNA abundance in the liver was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR). Results clearly showed that Hepc gene expression is upregulated by high dietary iron and downregulated when the dietary iron level is low. Both Hepc 1 and Hepc 2 expression responds coordinately to dietary iron. This work provides additional evidence of the key role of Hepc in the regulation of iron homeostasis.

Since experimental Se deficiency results in a significant increase in plasma cholesterol concentration the present investigation was undertaken to assess further the influence of this deficiency on the expression of proteins involved in hepatic lipid metabolism. Se deficiency was induced by feeding weanling male Wistar rats on a deficient diet for 6 weeks. Hypercholesterolaemia associated with Se deficiency was related to increased 3-hydroxy-3-methylglutaryl-coA (HMG-CoA) reductase (EC 1.1.1.34) activity in liver microsomes as compared with control animals. Hepatic lipoprotein receptor levels (LDL-receptor and HDL-binding proteins, HB1 and HB2) were not significantly affected by Se deficiency, as assessed by immunoblotting. Plasma triacylglycerol concentrations tended to decrease in Se-deficient rats in concert with their reduced post-Triton secretion. There was no significant effect of Se deficiency on the hepatic synthesis of apolipoproteins. These results point to the need for further investigations into the mechanism related to the increased activity of HMG-CoA reductase and the enhanced cholesterogenesis in the liver of Se-deficient rats likely to result from this.