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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2010-11-26
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pubmed:databankReference |
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pubmed:abstractText |
Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1?(-/-)?(f/f/MLC-Cre) mice) were generated and characterized. PGC-1?(-/-)?(f/f/MLC-Cre) mice exhibit a dramatic reduction in exercise performance compared to single PGC-1?- or PGC-1?-deficient mice and wild-type controls. The exercise phenotype of the PGC-1?(-/-)?(f/f/MLC-Cre) mice was associated with a marked diminution in muscle oxidative capacity, together with rapid depletion of muscle glycogen stores. In addition, the PGC-1?/?-deficient muscle exhibited mitochondrial structural derangements consistent with fusion/fission and biogenic defects. Surprisingly, the proportion of oxidative muscle fiber types (I, IIa) was not reduced in the PGC-1?(-/-)?(f/f/MLC-Cre) mice. Moreover, insulin sensitivity and glucose tolerance were not altered in the PGC-1?(-/-)?(f/f/MLC-Cre) mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1932-7420
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pubmed:author |
pubmed-author:ChenZhoujiZ,
pubmed-author:ColliaDeannaD,
pubmed-author:GengTuoyuT,
pubmed-author:KellyDaniel PDP,
pubmed-author:LeoneTeresa CTC,
pubmed-author:LongR LRL,
pubmed-author:RumseyJohn WJW,
pubmed-author:WozniakDavid FDF,
pubmed-author:YanZhenZ,
pubmed-author:ZechnerChristophC,
pubmed-author:ZechnerJuliet FJF
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pubmed:copyrightInfo |
Copyright © 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
633-42
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pubmed:dateRevised |
2011-6-1
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pubmed:meshHeading |
pubmed-meshheading:21109195-Analysis of Variance,
pubmed-meshheading:21109195-Animals,
pubmed-meshheading:21109195-Gene Expression Profiling,
pubmed-meshheading:21109195-Glucose Tolerance Test,
pubmed-meshheading:21109195-Insulin Resistance,
pubmed-meshheading:21109195-Mice,
pubmed-meshheading:21109195-Mice, Knockout,
pubmed-meshheading:21109195-Microscopy, Electron,
pubmed-meshheading:21109195-Mitochondria,
pubmed-meshheading:21109195-Muscle, Skeletal,
pubmed-meshheading:21109195-Oxygen Consumption,
pubmed-meshheading:21109195-Physical Conditioning, Animal,
pubmed-meshheading:21109195-Polymerase Chain Reaction,
pubmed-meshheading:21109195-Transcription Factors
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pubmed:year |
2010
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pubmed:articleTitle |
Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity.
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pubmed:affiliation |
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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