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Systemic regulation of intestinal iron absorption.
IUBMB Life. 2005 Jul; 57(7):499-503.IL

Abstract

The intestinal absorption of the essential trace element iron and its mobilization from storage sites in the body are controlled by systemic signals that reflect tissue iron requirements. Recent advances have indicated that the liver-derived peptide hepcidin plays a central role in this process by repressing iron release from intestinal enterocytes, macrophages and other body cells. When iron requirements are increased, hepcidin levels decline and more iron enters the plasma. It has been proposed that the level of circulating diferric transferrin, which reflects tissue iron levels, acts as a signal to alter hepcidin expression. In the liver, the proteins HFE, transferrin receptor 2 and hemojuvelin may be involved in mediating this signal as disruption of each of these molecules decreases hepcidin expression. Patients carrying mutations in these molecules or in hepcidin itself develop systemic iron loading (or hemochromatosis) due to their inability to down regulate iron absorption. Hepcidin is also responsible for the decreased plasma iron or hypoferremia that accompanies inflammation and various chronic diseases as its expression is stimulated by pro-inflammatory cytokines such as interleukin 6. The mechanisms underlying the regulation of hepcidin expression and how it acts on cells to control iron release are key areas of ongoing research.

Authors+Show Affiliations

Iron Metabolism Laboratory, Queensland Institute of Medical Research, Brisbane, Queensland, Australia.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16081371

Citation

Steele, Teresa M., et al. "Systemic Regulation of Intestinal Iron Absorption." IUBMB Life, vol. 57, no. 7, 2005, pp. 499-503.
Steele TM, Frazer DM, Anderson GJ. Systemic regulation of intestinal iron absorption. IUBMB Life. 2005;57(7):499-503.
Steele, T. M., Frazer, D. M., & Anderson, G. J. (2005). Systemic regulation of intestinal iron absorption. IUBMB Life, 57(7), 499-503.
Steele TM, Frazer DM, Anderson GJ. Systemic Regulation of Intestinal Iron Absorption. IUBMB Life. 2005;57(7):499-503. PubMed PMID: 16081371.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Systemic regulation of intestinal iron absorption. AU - Steele,Teresa M, AU - Frazer,David M, AU - Anderson,Gregory J, PY - 2005/8/6/pubmed PY - 2006/10/27/medline PY - 2005/8/6/entrez SP - 499 EP - 503 JF - IUBMB life JO - IUBMB Life VL - 57 IS - 7 N2 - The intestinal absorption of the essential trace element iron and its mobilization from storage sites in the body are controlled by systemic signals that reflect tissue iron requirements. Recent advances have indicated that the liver-derived peptide hepcidin plays a central role in this process by repressing iron release from intestinal enterocytes, macrophages and other body cells. When iron requirements are increased, hepcidin levels decline and more iron enters the plasma. It has been proposed that the level of circulating diferric transferrin, which reflects tissue iron levels, acts as a signal to alter hepcidin expression. In the liver, the proteins HFE, transferrin receptor 2 and hemojuvelin may be involved in mediating this signal as disruption of each of these molecules decreases hepcidin expression. Patients carrying mutations in these molecules or in hepcidin itself develop systemic iron loading (or hemochromatosis) due to their inability to down regulate iron absorption. Hepcidin is also responsible for the decreased plasma iron or hypoferremia that accompanies inflammation and various chronic diseases as its expression is stimulated by pro-inflammatory cytokines such as interleukin 6. The mechanisms underlying the regulation of hepcidin expression and how it acts on cells to control iron release are key areas of ongoing research. SN - 1521-6543 UR - https://www.unboundmedicine.com/medline/citation/16081371/full_citation L2 - https://doi.org/10.1080/15216540500149904 DB - PRIME DP - Unbound Medicine ER -
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