Muscle-specific Pparg deletion causes insulin resistance View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-12

AUTHORS

Andrea L Hevener, Weimin He, Yaacov Barak, Jamie Le, Gautam Bandyopadhyay, Peter Olson, Jason Wilkes, Ronald M Evans, Jerrold Olefsky

ABSTRACT

Thiazolidinediones (TZDs) are insulin-sensitizing drugs and are potent agonists of the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Although muscle is the major organ responsible for insulin-stimulated glucose disposal, PPAR-gamma is more highly expressed in adipose tissue than in muscle. To address this issue, we used the Cre-loxP system to knock out Pparg, the gene encoding PPAR-gamma, in mouse skeletal muscle. As early as 4 months of age, mice with targeted disruption of PPAR-gamma in muscle showed glucose intolerance and progressive insulin resistance. Using the hyperinsulinemic-euglycemic clamp technique, the in vivo insulin-stimulated glucose disposal rate (IS-GDR) was reduced by approximately 80% and was unchanged by 3 weeks of TZD treatment. These effects reveal a crucial role for muscle PPAR-gamma in the maintenance of skeletal muscle insulin action, the etiology of insulin resistance and the action of TZDs. More... »

PAGES

1491-1497

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm956

DOI

http://dx.doi.org/10.1038/nm956

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1052471478

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14625542


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