Duodenal HFE expression and hepcidin levels determine body iron homeostasis: modulation by genetic diversity and dietary iron availability

No abstract is available for this paper.

• Publication year

  2004

• Venue

  Journal of molecular medicine

• Publication date

  2004-05-13

• Fields of study

  Biology, Medicine, Environmental Science

• Identifiers
  DOI 10.1007/s00109-004-0542-3PMID 15173932
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation.

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• Inactivation of the hemochromatosis gene differentially regulates duodenal expression of iron-related mRNAs between mouse strains.

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• Hepcidin expression inversely correlates with the expression of duodenal iron transporters and iron absorption in rats.

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• Intestinal iron uptake determined by divalent metal transporter is enhanced in HFE-deficient mice with hemochromatosis.

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• Expression of the duodenal iron transporters divalent-metal transporter 1 and ferroportin 1 in iron deficiency and iron overload.

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• Iron‐dependent regulation of the divalent metal ion transporter

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• Hepcidin, a Urinary Antimicrobial Peptide Synthesized in the Liver*

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• Hepcidin: A putative iron-regulatory hormone relevant to hereditary hemochromatosis and the anemia of chronic disease

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