Document Detail


Energy metabolism in uncoupling protein 3 gene knockout mice.
MedLine Citation:
PMID:  10748196     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined.
Authors:
A J Vidal-Puig; D Grujic; C Y Zhang; T Hagen; O Boss; Y Ido; A Szczepanik; J Wade; V Mootha; R Cortright; D M Muoio; B B Lowell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  275     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2000 May 
Date Detail:
Created Date:  2000-06-30     Completed Date:  2000-06-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  16258-66     Citation Subset:  IM; S    
Affiliation:
Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Temperature / genetics
Body Weight / genetics
Carrier Proteins / genetics*,  metabolism
Eating
Energy Metabolism / genetics*
Female
Gene Targeting
Ion Channels
Male
Membrane Proteins / metabolism
Membrane Transport Proteins*
Mice
Mice, Knockout
Mitochondria, Muscle / metabolism
Mitochondrial Proteins*
Muscle, Skeletal / metabolism
Oxygen Consumption
Phenotype
Physical Conditioning, Animal
Proteins / metabolism
RNA, Messenger / metabolism
Reactive Oxygen Species / metabolism
Grant Support
ID/Acronym/Agency:
DK49569/DK/NIDDK NIH HHS; P30 DK46200/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Ion Channels; 0/Membrane Proteins; 0/Membrane Transport Proteins; 0/Mitochondrial Proteins; 0/Proteins; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/mitochondrial uncoupling protein; 0/mitochondrial uncoupling protein 2; 0/mitochondrial uncoupling protein 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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