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Mechanisms of the Depot Specificity of Peroxisome Proliferator–Activated Receptor Action on Adipose Tissue Metabolism

¹ Laval Hospital Research Centre and Department of Anatomy and Physiology, Faculty of Medicine, Laval University, Quebec, Quebec, Canada
² Department of Metabolic Disorders, Merck Research Laboratories, Rahway, New Jersey

Address correspondence and reprint requests to Dr. Yves Deshaies, Laval Hospital Research Centre, Laval Hospital–d’Youville Y3110, 2725 Ch Sainte-Foy, Quebec, QC, Canada G1V 4G5. E-mail: yves.deshaies{at}phs.ulaval.ca

Abbreviations: Acadl, long-chain acyl-CoA dehydrogenase; ATGL, adipose triglyceride lipase; DGAT-1, diacylglycerol acyltransferase 1; GyK, glycerol kinase; KRB, Krebs-Ringer bicarbonate; LPL, lipoprotein lipase; mCPT-1, muscle-type carnitine palmitoyltransferase 1; NEFA, nonesterified fatty acid; PDK, pyruvate dehydrogenase kinase; PGC-1, peroxisome proliferator–activated receptor coactivator 1; PPAR, peroxisome proliferator–activated receptor; TZD, thiazolidinedione; UCP-1, uncoupling protein 1; WAT, white adipose tissue

In this study, we aimed to establish the mechanisms whereby peroxisome proliferator–activated receptor (PPAR) agonism brings about redistribution of fat toward subcutaneous depots and away from visceral fat. In rats treated with the full PPAR agonist COOH (30 mg · kg^–1 · day^–1) for 3 weeks, subcutaneous fat mass was doubled and that of visceral fat was reduced by 30% relative to untreated rats. Uptake of triglyceride-derived nonesterified fatty acids was greatly increased in subcutaneous fat (14-fold) and less so in visceral fat (4-fold), with a concomitant increase, restricted to subcutaneous fat only, in mRNA levels of the uptake-, retention-, and esterification-promoting enzymes lipoprotein lipase, aP2, and diacylglycerol acyltransferase 1. Basal lipolysis and fatty acid recycling were stimulated by COOH in both subcutaneous fat and visceral fat, with no frank quantitative depot specificity. The agonist increased mRNA levels of enzymes of fatty acid oxidation and thermogenesis much more strongly in visceral fat than in subcutaneous fat, concomitantly with a stronger elevation in O₂ consumption in the former than in the latter. Mitochondrial biogenesis was stimulated equally in both depots. These findings demonstrate that PPAR agonism redistributes fat by stimulating the lipid uptake and esterification potential in subcutaneous fat, which more than compensates for increased O₂ consumption; conversely, lipid uptake is minimally altered and energy expenditure is greatly increased in visceral fat, with consequent reduction in fat accumulation.

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