Regulation of Iron Metabolism by Hepcidin

Hepcidin, a peptide hormone made in the liver, is the principal regulator of systemic iron homeostasis. Hepcidin controls plasma iron concentration and tissue distribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores. Hepc...

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Bibliographic Details
Published in:Annual review of nutrition 2006-01, Vol.26 (1), p.323-342
Main Authors: Nemeth, E, Ganz, T
Format: Article
Language:English
Subjects:
Antimicrobial Cationic Peptides - genetics
Antimicrobial Cationic Peptides - metabolism
Antimicrobial Cationic Peptides - physiology
Biological and medical sciences
dietary minerals
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Hemochromatosis - genetics
Hemochromatosis - metabolism
Hepcidins
Homeostasis
Humans
Inflammation - complications
Inflammation - metabolism
Iron - metabolism
iron absorption
iron homeostasis
Iron Metabolism Disorders - metabolism
literature reviews
liver
macrophages
peptide hormones
regulatory proteins
Vertebrates: anatomy and physiology, studies on body, several organs or systems
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Summary:Hepcidin, a peptide hormone made in the liver, is the principal regulator of systemic iron homeostasis. Hepcidin controls plasma iron concentration and tissue distribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores. Hepcidin acts by inhibiting cellular iron efflux through binding to and inducing the degradation of ferroportin, the sole known cellular iron exporter. Synthesis of hepcidin is homeostatically increased by iron loading and decreased by anemia and hypoxia. Hepcidin is also elevated during infections and inflammation, causing a decrease in serum iron levels and contributing to the development of anemia of inflammation, probably as a host defense mechanism to limit the availability of iron to invading microorganisms. At the opposite side of the spectrum, hepcidin deficiency appears to be the ultimate cause of most forms of hemochromatosis, either due to mutations in the hepcidin gene itself or due to mutations in the regulators of hepcidin synthesis. The emergence of hepcidin as the pathogenic factor in most systemic iron disorders should provide important opportunities for improving their diagnosis and treatment.
ISSN:0199-9885
1545-4312
DOI:10.1146/annurev.nutr.26.061505.111303