| High dietary iron reduces transporters involved in iron and manganese metabolism and increases intestinal permeability in calves. | |
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MedLine Citation:
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PMID: 20105537 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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A 56-d experiment was designed to examine the effect of high dietary Fe on metal transporters involved in Fe and Mn metabolism. Fourteen weaned Holstein calves were stratified by weight and randomly assigned to 1 of 2 treatments: 1) no supplemental Fe (normal Fe) or 2) 750mg of supplemental Fe/kg of dry matter (high Fe). Jugular blood was collected on d 0, 35, and 56. At the end of the trial, 6 calves per treatment were humanely killed and duodenal scrapings, liver, and heart were collected for analysis. Additionally, proximal duodenum was mounted on Ussing chambers to assess intestinal barrier integrity. Calves receiving high dietary Fe displayed decreased transepithelial resistance and increased apical-to-basolateral flux of radiolabeled mannitol, suggesting that high Fe created increased intestinal permeability. Feeding calves a diet high in Fe decreased average daily gain, dry matter intake, and feed efficiency. Hemoglobin and serum Fe concentrations did not differ due to dietary treatment. High dietary Fe increased concentrations of Fe in the liver, but did not affect heart or duodenal Fe concentrations. Duodenal Mn concentrations were lowered by feeding a high Fe diet, but liver and heart Mn concentrations were not affected. As determined by real-time reverse transcription PCR, relative hepatic expression of the gene that encodes the Fe regulatory hormone hepcidin was 5-fold greater in calves fed high dietary Fe. Hepcidin is released in response to increased Fe status and binds to the Fe export protein ferroportin causing ferroportin to be degraded, thereby reducing dietary Fe absorption. Confirmation of this result was achieved through Western blotting of duodenal protein, which revealed that ferroportin was decreased in calves fed high dietary Fe. Duodenal protein expression of divalent metal transporter 1 (DMT1), a Fe import protein that can also transport Mn, tended to be reduced by high dietary Fe. Transcript levels of several genes involved in Fe metabolism in liver and duodenum were unchanged by treatment. In summary, feeding calves a diet high in Fe induced a signal cascade (hepcidin) designed to reduce absorption of Fe (via reduced protein expression of ferroportin and DMT1) in a manner similar to that reported in rodents. Additionally, reduced levels of DMT1 protein appeared to decrease duodenal Mn, suggesting that Mn may also be a substrate for DMT1 in cattle. |
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Authors:
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S L Hansen; M S Ashwell; A J Moeser; R S Fry; M D Knutson; J W Spears |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of dairy science Volume: 93 ISSN: 1525-3198 ISO Abbreviation: J. Dairy Sci. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-28 Completed Date: 2010-04-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985126R Medline TA: J Dairy Sci Country: United States |
Other Details:
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Languages: eng Pagination: 656-65 Citation Subset: IM |
Copyright Information:
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Copyright 2010 American Dairy Science Association. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Animal Science, North Carolina State University, Raleigh, NC 27695-7621, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight / physiology Cattle / metabolism, physiology* Diet / veterinary* Duodenum / chemistry, drug effects Gene Expression Regulation / drug effects Heart / drug effects Iron / analysis, blood, metabolism* Iron, Dietary / metabolism*, pharmacology Liver / drug effects, metabolism Male Manganese / analysis, blood, metabolism* Membrane Transport Proteins / metabolism Myocardium / chemistry Oxidative Stress / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Iron, Dietary; 0/Membrane Transport Proteins; 7439-89-6/Iron; 7439-96-5/Manganese |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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