AI Article Synopsis
- Hepcidin inhibits iron (Fe) absorption and recycling by targeting specific proteins, with its disruption leading to increased Fe uptake in mice.
- Hepcidin injections blocked Fe absorption more effectively in mice lacking hepcidin (Hepc1-/-) while also decreasing iron-exporting proteins in key organs.
- The study highlights that hepcidin's regulatory effects on Fe absorption can be overruled by dietary Fe deficiency, suggesting its influence varies with iron levels in the diet.
Article Abstract
Hepcidin, the Fe-regulatory peptide, has been shown to inhibit Fe absorption and reticuloendothelial Fe recycling. The present study was conducted to explore the mechanism of in vivo Fe regulation through genetic disruption of hepcidin1 and acute effects of hepcidin treatment in hepcidin1 knockout (Hepc1-/-) and heterozygous mice. Hepcidin1 disruption resulted in significantly increased intestinal Fe uptake. Hepcidin injection inhibited Fe absorption in both genotypes, but the effects were more evident in the knockout mice. Hepcidin administration was also associated with decreased membrane localisation of ferroportin in the duodenum, liver and, most significantly, in the spleen of Hepc1-/- mice. Hypoferraemia was induced in heterozygous mice by hepcidin treatment, but not in Hepc1-/- mice, 4 h after injection. Interestingly, Fe absorption and serum Fe levels in Hepc1-/- and heterozygous mice fed a low-Fe diet were not affected by hepcidin injection. The present study demonstrates that hepcidin deficiency causes increased Fe absorption. The effects of hepcidin were abolished by dietary Fe deficiency, indicating that the response to hepcidin may be influenced by dietary Fe level or Fe status.
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| http://dx.doi.org/10.1017/S0007114510005507 | DOI Listing |
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Article Synopsis
- Hepcidin, a hormone crucial for iron regulation, is shown to play a role in liver fibrosis by preventing hepatocyte apoptosis via the PERK pathway.
- A study using CCl4-induced liver fibrosis in hepcidin knockout mice revealed that the absence of hepcidin led to more severe liver damage and increased apoptosis compared to wild-type mice.
- Transcriptomic analysis identified that the PERK molecule is upregulated in the absence of hepcidin, suggesting its involvement in regulating cell death in liver injury, highlighting hepcidin's potential as a therapeutic target for liver fibrosis.
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