Source:http://linkedlifedata.com/resource/pubmed/id/15701680
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2005-6-16
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pubmed:abstractText |
Insulin resistance in skeletal muscle and heart plays a major role in the development of type 2 diabetes and diabetic heart failure and may be causally associated with altered lipid metabolism. Hormone-sensitive lipase (HSL) is a rate-determining enzyme in the hydrolysis of triglyceride in adipocytes, and HSL-deficient mice have reduced circulating fatty acids and are resistant to diet-induced obesity. To determine the metabolic role of HSL, we examined the changes in tissue-specific insulin action and glucose metabolism in vivo during hyperinsulinemic euglycemic clamps after 3 wk of high-fat or normal chow diet in awake, HSL-deficient (HSL-KO) mice. On normal diet, HSL-KO mice showed a twofold increase in hepatic insulin action but a 40% decrease in insulin-stimulated cardiac glucose uptake compared with wild-type littermates. High-fat feeding caused a similar increase in whole body fat mass in both groups of mice. Insulin-stimulated glucose uptake was reduced by 50-80% in skeletal muscle and heart of wild-type mice after high-fat feeding. In contrast, HSL-KO mice were protected from diet-induced insulin resistance in skeletal muscle and heart, and these effects were associated with reduced intramuscular triglyceride and fatty acyl-CoA levels in the fat-fed HSL-KO mice. Overall, these findings demonstrate the important role of HSL on skeletal muscle, heart, and liver glucose metabolism.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0193-1849
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pubmed:author |
pubmed-author:ClineGaryG,
pubmed-author:DongJianyingJ,
pubmed-author:HigashimoriTakamasaT,
pubmed-author:KimHyo-JeongHJ,
pubmed-author:KimJason KJK,
pubmed-author:KimYoon-JungYJ,
pubmed-author:LiHongH,
pubmed-author:MitchellGrant AGA,
pubmed-author:ParkSo-YoungSY,
pubmed-author:PrentkiMarcM,
pubmed-author:ShulmanGerald IGI,
pubmed-author:WangShupeiS
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pubmed:issnType |
Print
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pubmed:volume |
289
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E30-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15701680-Adaptation, Physiological,
pubmed-meshheading:15701680-Adipose Tissue,
pubmed-meshheading:15701680-Animals,
pubmed-meshheading:15701680-Dietary Fats,
pubmed-meshheading:15701680-Glucose,
pubmed-meshheading:15701680-Insulin,
pubmed-meshheading:15701680-Insulin Resistance,
pubmed-meshheading:15701680-Liver,
pubmed-meshheading:15701680-Male,
pubmed-meshheading:15701680-Mice,
pubmed-meshheading:15701680-Mice, Knockout,
pubmed-meshheading:15701680-Muscle, Skeletal,
pubmed-meshheading:15701680-Myocardium,
pubmed-meshheading:15701680-Organ Specificity,
pubmed-meshheading:15701680-Sterol Esterase
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pubmed:year |
2005
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pubmed:articleTitle |
Hormone-sensitive lipase knockout mice have increased hepatic insulin sensitivity and are protected from short-term diet-induced insulin resistance in skeletal muscle and heart.
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pubmed:affiliation |
Department of Internal Medicine, Section of Endocrinology and Metabolism, Yale University School of Medicine, New Haven, CT 06520-8020, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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