Document Detail


Decreased mitochondrial proton leak and reduced expression of uncoupling protein 3 in skeletal muscle of obese diet-resistant women.
MedLine Citation:
PMID:  12145158     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Weight loss in response to caloric restriction is variable. Because skeletal muscle mitochondrial proton leak may account for a large proportion of resting metabolic rate, we compared proton leak in diet-resistant and diet-responsive overweight women and compared the expression and gene characteristics of uncoupling protein (UCP)2 and UCP3. Of 1,129 overweight women who completed the University of Ottawa Weight Management Clinic program, 353 met compliance criteria and were free of medical conditions that could affect weight loss. Subjects were ranked according to percent body weight loss during the first 6 weeks of a 900-kcal meal replacement protocol. The highest and lowest quintiles of weight loss were defined as diet responsive and diet resistant, respectively. After body weight had been stable for at least 10 weeks, 12 of 70 subjects from each group consented to muscle biopsy and blood sampling for determinations of proton leak, UCP mRNA expression, and genetic studies. Despite similar baseline weight and age, weight loss was 43% greater, mitochondrial proton leak-dependent (state 4) respiration was 51% higher (P = 0.0062), and expression of UCP3 mRNA abundance was 25% greater (P < 0.001) in diet-responsive than in diet-resistant subjects. There were no differences in UCP2 mRNA abundance. None of the known polymorphisms in UCP3 or its 5' flanking sequence were associated with weight loss or UCP3 mRNA abundance. Thus, proton leak and the expression of UCP3 correlate with weight loss success and may be candidates for pharmacological regulation of fat oxidation in obese diet-resistant subjects.
Authors:
Mary-Ellen Harper; Robert Dent; Shadi Monemdjou; Véronic Bézaire; Lloyd Van Wyck; George Wells; Gul Nihan Kavaslar; Andre Gauthier; Frédérique Tesson; Ruth McPherson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Diabetes     Volume:  51     ISSN:  0012-1797     ISO Abbreviation:  Diabetes     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-07-29     Completed Date:  2002-08-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2459-66     Citation Subset:  AIM; IM    
Affiliation:
Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Faculty of Medicine, Ottawa, Ontarion, Canada. mharper@uottawa.ca
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MeSH Terms
Descriptor/Qualifier:
Body Weight
Carrier Proteins / genetics*
DNA Primers
Diet, Reducing
Energy Intake
Female
Gene Expression Regulation*
Genetic Testing
Humans
Hydrogen-Ion Concentration*
Ion Channels
Membrane Transport Proteins*
Mitochondria, Muscle / metabolism*
Mitochondrial Proteins*
Muscle, Skeletal / metabolism*
Obesity / genetics*
Oxygen Consumption
Proteins / genetics*
Protons
RNA, Messenger / genetics
Transcription, Genetic
Treatment Failure
Weight Loss / genetics*
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/DNA Primers; 0/Ion Channels; 0/Membrane Transport Proteins; 0/Mitochondrial Proteins; 0/Proteins; 0/Protons; 0/RNA, Messenger; 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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