Disorders of iron metabolism. Part 1: molecular basis of iron homoeostasis
Iron functionsIron is an essential micronutrient, as it is required for satisfactory erythropoietic function, oxidative metabolism and cellular immune response.Iron physiologyAbsorption of dietary iron (1–2 mg/day) is tightly regulated and just balanced against iron loss because there are no active...
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Published in | Journal of clinical pathology Vol. 64; no. 4; pp. 281 - 286 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and Association of Clinical Pathologists
01.04.2011
BMJ Publishing Group BMJ Publishing Group LTD |
Subjects | |
Online Access | Get full text |
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Summary: | Iron functionsIron is an essential micronutrient, as it is required for satisfactory erythropoietic function, oxidative metabolism and cellular immune response.Iron physiologyAbsorption of dietary iron (1–2 mg/day) is tightly regulated and just balanced against iron loss because there are no active iron excretory mechanisms. Dietary iron is found in haem (10%) and non-haem (ionic, 90%) forms, and their absorption occurs at the apical surface of duodenal enterocytes via different mechanisms. Iron is exported by ferroportin 1 (the only putative iron exporter) across the basolateral membrane of the enterocyte into the circulation (absorbed iron), where it binds to transferrin and is transported to sites of use and storage. Transferrin-bound iron enters target cells—mainly erythroid cells, but also immune and hepatic cells—via receptor-mediated endocytosis. Senescent erythrocytes are phagocytosed by reticuloendothelial system macrophages, haem is metabolised by haem oxygenase, and the released iron is stored as ferritin. Iron will be later exported from macrophages to transferrin. This internal turnover of iron is essential to meet the requirements of erythropoiesis (20–30 mg/day). As transferrin becomes saturated in iron-overload states, excess iron is transported to the liver, the other main storage organ for iron, carrying the risk of free radical formation and tissue damage.Regulation of iron homoeostasisHepcidin, synthesised by hepatocytes in response to iron concentrations, inflammation, hypoxia and erythropoiesis, is the main iron-regulatory hormone. It binds ferroportin on enterocytes, macrophages and hepatocytes triggering its internalisation and lysosomal degradation. Inappropriate hepcidin secretion may lead to either iron deficiency or iron overload. |
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Bibliography: | local:jclinpath;64/4/281 ark:/67375/NVC-G5448NPT-9 href:jclinpath-64-281.pdf ArticleID:jclinpath79046 All author contributed equally to the design, writing and discussion of this paper. PMID:21177266 istex:4A5DA2C3FCDA2B8CE0234DFF05EDD49341A3C3B7 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0021-9746 1472-4146 |
DOI: | 10.1136/jcp.2010.079046 |