rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2011-7-4
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pubmed:databankReference |
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pubmed:abstractText |
Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-?/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3-deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3(-)(/-) white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3(-/-) adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-1? expression. We observe significant correlation between TGF-?1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-? signaling protects mice from obesity, diabetes, and hepatic steatosis. Together, these results demonstrate that TGF-? signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-? activity might be an effective treatment strategy for obesity and diabetes.
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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 |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jul
|
pubmed:issn |
1932-7420
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pubmed:author |
pubmed-author:ChenWeipingW,
pubmed-author:DuanZhigangZ,
pubmed-author:FinkelTorenT,
pubmed-author:GavrilovaOksanaO,
pubmed-author:KamarajuAnil KAK,
pubmed-author:LonningScottS,
pubmed-author:MalekRanaR,
pubmed-author:QuijanoCeliaC,
pubmed-author:RaneSushil GSG,
pubmed-author:SkarulisMonicaM,
pubmed-author:StueltenChristinaC,
pubmed-author:SumnerAnne EAE,
pubmed-author:SunPeterP,
pubmed-author:WrightElizabeth CEC,
pubmed-author:YadavHariomH,
pubmed-author:ZerfasPatriciaP
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pubmed:copyrightInfo |
Copyright © 2011 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
6
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pubmed:volume |
14
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
67-79
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pubmed:meshHeading |
pubmed-meshheading:21723505-Adipose Tissue, Brown,
pubmed-meshheading:21723505-Adipose Tissue, White,
pubmed-meshheading:21723505-Animals,
pubmed-meshheading:21723505-Antibodies,
pubmed-meshheading:21723505-DNA-Binding Proteins,
pubmed-meshheading:21723505-Diabetes Mellitus,
pubmed-meshheading:21723505-Energy Metabolism,
pubmed-meshheading:21723505-Glucose Tolerance Test,
pubmed-meshheading:21723505-Mice,
pubmed-meshheading:21723505-Mice, Knockout,
pubmed-meshheading:21723505-Mice, Obese,
pubmed-meshheading:21723505-Mitochondria,
pubmed-meshheading:21723505-Obesity,
pubmed-meshheading:21723505-Signal Transduction,
pubmed-meshheading:21723505-Smad3 Protein,
pubmed-meshheading:21723505-Trans-Activators,
pubmed-meshheading:21723505-Transcription Factors,
pubmed-meshheading:21723505-Transforming Growth Factor beta
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pubmed:year |
2011
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pubmed:articleTitle |
Protection from obesity and diabetes by blockade of TGF-?/Smad3 signaling.
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pubmed:affiliation |
Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Clinical Research Center, South Drive and Old Georgetown Road, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Intramural
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