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J. Lipid Res.
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A more recent version of this article appeared on June 1, 2009

Papers In Press, published online ahead of print February 5, 2009
J. Lipid Res., doi:10.1194/jlr.M800620-JLR200
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Submitted on December 2, 2008
Revised on January 29, 2009
Accepted on February 5, 2009

Depot-specific effects of the PPARgamma agonist rosiglitazone on adipose tissue glucose uptake and metabolism

William T. Festuccia, Pierre-Gilles Blanchard, Véronique Turcotte, Mathieu Laplante, Meltem Sariahmetoglu, David N. Brindley, and Yves Deshaies

Laval Hospital Research Center, Laval University, Quebec, Quebec G1V 4G5

Corresponding Author: yves.deshaies{at}phs.ulaval.ca

We investigated mechanisms whereby PPARgamma agonism redistributes lipid from visceral fat (VF) toward subcutaneous fat (SF) by studying the impact of PPARgamma activation on VF and SF glucose uptake and metabolism, lipogenesis and mRNA levels and activity of enzymes involved in triacylglycerol (TAG) synthesis. VF (retroperitoneal) and SF (inguinal) of rats treated or not for 7 days with rosiglitazone (15 mg/kg/day) were evaluated in vivo for glucose uptake and lipogenesis and in vitro for glucose metabolism, gene expression, and activities of glycerolphosphate acyltransferase (GPAT), phosphatidate phosphatase-1 (PAP1 or lipin-1) and diacylglycerol acyltransferase (DGAT). Rosiglitazone increased SF glucose uptake, GLUT4 mRNA and insulin-stimulated glucose oxidation, conversion to lactate, glycogen, and the glycerol and fatty acid components of TAG. In VF, only glucose incorporation into TAG-glycerol was stimulated by rosiglitazone, and to a lesser extent than in SF (1.5 vs. 3-fold, respectively). mRNA levels of proteins involved in glycolysis, Krebs cycle, glycogen synthesis and lipogenesis were markedly upregulated by rosiglitazone in SF, but less so in VF. Rosiglitazone-induced activation of TAG-glycerol synthesis in vivo (2.8 vs 1.9-fold, respectively) and lipin activity (4.6 vs. 1.5-fold) was much more marked in SF than VF, whereas GPAT activity was increased similarly in both depots. The preferential increase in glucose uptake and intracellular metabolism in SF contributes to the redistribution of TAG from VF to SF induced by PPARgamma agonists, which in turn favors global insulin sensitization.


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