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This version published online on December 5, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-1268
A more recent version of this article appeared on February 1, 2007
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Submitted on June 14, 2006
Accepted on November 29, 2006

Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) and adipose tissue -- understanding obesity-related changes in regulation of lipid and glucose metabolism

Arya M. Sharma* and Bart Staels

Canada Research Chair for Cardiovascular Obesity Research and Management, McMaster University, Hamilton, ON; Institut Pasteur de Lille, Département d'Athérosclérose, Lille, F-59019 France; Inserm U545, Lille, F-509019 France; Université de Lille 2, Lille, F-59006 France

* To whom correspondence should be addressed. 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 -- adipocytes display morphological differences alongside aberrant endocrine and metabolic function and low-grade inflammation.

Evidence Acquisition: Articles on the role of PPAR{gamma} 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{gamma} 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{gamma} is highly expressed in adipose tissue, where its activation with thiazolidinediones alters fat topography, adipocyte phenotype, and upregulates genes involved in fatty acid metabolism and triglyceride storage. Furthermore, PPAR{gamma} activation is associated with potentially beneficial effects on the expression and secretion of a range of factors including adiponectin, resistin, IL-6, TNF{alpha}, PAI-1, MCP-1 and angiotensinogen, as well as a reduction in plasma NEFA supply. The effects of PPAR{gamma} also extend to macrophages, where they suppress production of inflammatory mediators. As such, PPAR{gamma} activation appears to have a beneficial effect on the relationship between the macrophage and adipocyte that is distorted in obesity. Thus, PPAR{gamma} activating ligands improve adipose tissue function and may have a role in preventing progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis.
Key words: PPAR{gamma} • adipose tissue • thiazolidinediones • lipid metabolism • glucose metabolism




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