Document Detail

Uncoupling protein 3 and fatty acid metabolism.
MedLine Citation:
PMID:  11709075     Owner:  NLM     Status:  MEDLINE    
A role for uncoupling protein (UCP) 3 in fatty acid metabolism is reviewed within the context of our proposal, first put forward in 1998, that this homologue of UCP1 may be involved in the regulation of lipids as fuel substrate rather than in the mediation of thermogenesis. Since then, the demonstrations of muscle-type differences in UCP3 gene regulation in response to dietary manipulations (starvation, high-fat feeding) or to pharmacological interferences with the flux of lipid substrates between adipose-tissue stores and skeletal-muscle mitochondrial oxidation are all in accord with this proposed role for UCP3 in regulating lipids as fuel substrate. However, given the current limitations of gene-knockout technology for evaluating/interpreting the functional importance of genes encoding mitochondrial membrane proteins, the transition from 'associative' to 'cause-and-effect' evidence for a physiological role of UCP3 in regulating fatty acid metabolism will have to await the development of assays that are sensitive to changes in UCP3 activity. Furthermore, in evaluating the physiological regulators of UCP3, the available evidence points to the existence of adipose-derived factor(s) which, independently of circulating levels of free fatty acids, initiates events leading to the transcription of genes encoding UCP3 and key enzymes of lipid oxidation in the fast glycolytic or fast oxidative-glycolytic muscles, i.e. in the bulk of the skeletal-muscle mass. It is proposed that in tissues where UCP3 co-exists with UCP2 (skeletal muscle, brown adipose tissue, heart) they may act in concert in the overall regulation of lipid oxidation, concomitant to the prevention of lipid-induced oxidative damage.
A G Dulloo; S Samec; J Seydoux
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Biochemical Society transactions     Volume:  29     ISSN:  0300-5127     ISO Abbreviation:  Biochem. Soc. Trans.     Publication Date:  2001 Nov 
Date Detail:
Created Date:  2001-11-15     Completed Date:  2002-03-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7506897     Medline TA:  Biochem Soc Trans     Country:  England    
Other Details:
Languages:  eng     Pagination:  785-91     Citation Subset:  IM    
Institute of Physiology, Department of Medicine, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland.
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MeSH Terms
Adipose Tissue / metabolism
Carrier Proteins / metabolism*,  physiology*
Fatty Acids / metabolism*
Insulin Resistance
Ion Channels
Lipid Metabolism
Mitochondria / metabolism
Mitochondrial Proteins
Models, Biological
Muscle, Skeletal / metabolism
Reg. No./Substance:
0/Carrier Proteins; 0/Fatty Acids; 0/Ion Channels; 0/Mitochondrial Proteins; 0/mitochondrial uncoupling protein 3

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