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Peroxisome Proliferator-Activated Receptor and Adipose Tissue—Understanding Obesity-Related Changes in Regulation of Lipid and Glucose Metabolism

Canada Research Chair for Cardiovascular Obesity Research and Management (A.M.S.), McMaster University, Hamilton, Ontario, Canada L8L 2X2; Institut Pasteur de Lille (B.S.), Département d’Athérosclérose, F-59019 Lille, France; Institut National de la Santé et de la Recherche Médicale U545 (B.S.), F-509019 Lille, France; and Université de Lille 2 (B.S.), F-59006 Lille, France

Address all correspondence and requests for reprints to: Arya M. Sharma, M.D., FRCPC, Professor of Medicine, Canada Research Chair for Cardiovascular Obesity Research and Management, McMaster University, Hamilton General Hospital, 237 Barton Street East, Hamilton, Ontario, Canada L8L 2X2. E-mail: sharma{at}cardio.on.ca.

Context: Adipose tissue is a metabolically dynamic organ, serving as a buffer to control fatty acid flux and a regulator of endocrine function. In obese subjects, and those with type 2 diabetes or the metabolic syndrome, adipose tissue function is altered (i.e. adipocytes display morphological differences alongside aberrant endocrine and metabolic function and low-grade inflammation).

Evidence Acquisition: Articles on the role of peroxisome proliferator-activated receptor (PPAR) in adipose tissue of healthy individuals and those with obesity, metabolic syndrome, or type 2 diabetes were sourced using MEDLINE (1990–2006).

Evidence Synthesis: Articles were assessed to provide a comprehensive overview of how PPAR-activating ligands improve adipose tissue function, and how this links to improvements in insulin resistance and the progression to type 2 diabetes and atherosclerosis.

Conclusions: PPAR is highly expressed in adipose tissue, where its activation with thiazolidinediones alters fat topography and adipocyte phenotype and up-regulates genes involved in fatty acid metabolism and triglyceride storage. Furthermore, PPAR activation is associated with potentially beneficial effects on the expression and secretion of a range of factors, including adiponectin, resistin, IL-6, TNF, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, and angiotensinogen, as well as a reduction in plasma nonesterified fatty acid supply. The effects of PPAR also extend to macrophages, where they suppress production of inflammatory mediators. As such, PPAR activation appears to have a beneficial effect on the relationship between the macrophage and adipocyte that is distorted in obesity. Thus, PPAR-activating ligands improve adipose tissue function and may have a role in preventing progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis.

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