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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2006-8-16
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pubmed:abstractText |
We studied the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-alpha agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-alpha activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Dietary Carbohydrates,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Fenofibrate,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Lipids,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR alpha,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Resistin,
http://linkedlifedata.com/resource/pubmed/chemical/Triglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/adiponectin receptor 1, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/adiponectin receptor 2, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0013-7227
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
147
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4517-24
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16740970-Adiponectin,
pubmed-meshheading:16740970-Adipose Tissue,
pubmed-meshheading:16740970-Animals,
pubmed-meshheading:16740970-Blood Glucose,
pubmed-meshheading:16740970-Diet,
pubmed-meshheading:16740970-Dietary Carbohydrates,
pubmed-meshheading:16740970-Fatty Acids, Nonesterified,
pubmed-meshheading:16740970-Fatty Liver,
pubmed-meshheading:16740970-Fenofibrate,
pubmed-meshheading:16740970-Gene Expression,
pubmed-meshheading:16740970-Glucose Clamp Technique,
pubmed-meshheading:16740970-Insulin,
pubmed-meshheading:16740970-Insulin Resistance,
pubmed-meshheading:16740970-Lipids,
pubmed-meshheading:16740970-Liver,
pubmed-meshheading:16740970-Male,
pubmed-meshheading:16740970-Mice,
pubmed-meshheading:16740970-Mice, Inbred C57BL,
pubmed-meshheading:16740970-Muscle, Skeletal,
pubmed-meshheading:16740970-Obesity,
pubmed-meshheading:16740970-Organ Size,
pubmed-meshheading:16740970-PPAR alpha,
pubmed-meshheading:16740970-RNA, Messenger,
pubmed-meshheading:16740970-Receptors, Adiponectin,
pubmed-meshheading:16740970-Receptors, Cell Surface,
pubmed-meshheading:16740970-Resistin,
pubmed-meshheading:16740970-Triglycerides,
pubmed-meshheading:16740970-Weight Loss
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pubmed:year |
2006
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pubmed:articleTitle |
Improvement of insulin sensitivity after peroxisome proliferator-activated receptor-alpha agonist treatment is accompanied by paradoxical increase of circulating resistin levels.
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pubmed:affiliation |
Third Department of Medicine, First Faculty of Medicine and General University Hospital, Charles University, 128 08 Prague, Czech Republic. mhalu@lf1.cuni.cz
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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