Document Detail


Intestinal regulation of copper homeostasis: a developmental perspective.
MedLine Citation:
PMID:  18779306     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Stable-isotope studies in human infants and adults have shown that copper homeostasis occurs, but the contribution of the small intestine to this regulation is still not well understood. Copper first needs to be reduced to the cuprous form, most likely by Steap proteins on the apical membrane. Copper is subsequently absorbed by Ctr1 and then transferred in the enterocyte by the chaperone Atox1 to reach ATP7A for export from the cell. The role of ATP7B, shown to be present in the small intestine, is still poorly understood. In situations of high copper exposure, Ctr1 is endocytosed, metallothionein is induced, and ATP7A moves to a more basolateral localization. However, the ontogeny of regulation of copper homeostasis has received little attention. In rat pups, tissue copper and total-body (67)Cu retention decrease throughout postnatal development, whereas liver (67)Cu retention, serum copper, and ceruloplasmin activity increase. Total (67)Cu absorption decreases and intestinal (67)Cu retention increases with increased copper intake. During early infancy (day 10), copper supplementation increases intestinal copper and metallothionein gene expression, and Ctr1 protein levels increase, whereas Atp7A and Atp7B are unaffected. However, during late infancy (day 20), intestinal copper concentrations are unaffected by supplementation, but Ctr1, ATP7A, and Atp7B protein levels are higher than in controls. Thus, maturation of small intestine copper transport occurs through increased abundance and altered localization of Ctr1, Atp7A, and Atp7B. The mechanisms behind this maturation, including both transcriptional and posttranscriptional regulation, require further studies.
Authors:
Bo Lönnerdal
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of clinical nutrition     Volume:  88     ISSN:  1938-3207     ISO Abbreviation:  Am. J. Clin. Nutr.     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-09-09     Completed Date:  2008-10-09     Revised Date:  2009-05-15    
Medline Journal Info:
Nlm Unique ID:  0376027     Medline TA:  Am J Clin Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  846S-50S     Citation Subset:  AIM; IM    
Affiliation:
Department of Nutrition, University of California, Davis, CA 95616, USA. bllonnerdal@ucdavis.edu
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphatases / metabolism
Animals
Animals, Suckling / metabolism
Biological Transport
Caco-2 Cells / metabolism
Carrier Proteins / metabolism
Cation Transport Proteins / metabolism
Cell Line, Tumor
Copper / deficiency,  metabolism*,  pharmacology
Homeostasis
Humans
Intestines / growth & development,  metabolism*
Rats
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Cation Transport Proteins; 7440-50-8/Copper; EC 3.6.1.-/Adenosine Triphosphatases; EC 3.6.3.4/ATP7A protein, human

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