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INVITED REVIEW

PPARs and the kidney in metabolic syndrome

¹Center for Nephrology, University College of London, London, United Kingdom; ²Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York; ³Department of Physiology and Pathophysiology, Peking (Beijing) University Health Science Center, Beijing, China; and ⁴Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee

Submitted 31 March 2007 ; accepted in final form 22 January 2008

The metabolic syndrome (MetS) is defined by a set of metabolic risk factors, including insulin resistance, central obesity, dyslipidemia, hyperglycemia, and hypertension for type 2 diabetes and cardiovascular disease. Although both retrospective and prospective clinical studies have revealed that MetS is associated with chronic renal disease, even with a nondiabetic cause, the cellular and molecular mechanisms in this association remain largely uncharacterized. Recently, increasing evidence suggests that peroxisome proliferator-activated receptors (PPARs), a subgroup of the nuclear hormone receptor superfamily of ligand-activated transcription factors, may play an important role in the pathogenesis of MetS. All three members of the PPAR nuclear receptor subfamily, PPAR, -β/, and -, are critical in regulating insulin sensitivity, adipogenesis, lipid metabolism, inflammation, and blood pressure. PPARs have also been implicated in many renal pathophysiological conditions, including diabetic nephropathy and glomerulosclerosis. Ligands for PPARs such as hypolipidemic PPAR activators, and antidiabetic thiazolidinedione PPAR agonists affect not only diverse aspects of MetS but also renal disease progression. Emerging data suggest that PPARs may be potential therapeutic targets for MetS and its related renal complications. This review focuses on current knowledge of the role of PPARs in MetS and discusses the potential therapeutic utility of PPAR modulators in the treatment of kidney diseases associated with MetS.

nuclear receptor; insulin-resistance syndrome; syndrome X; kidney disease

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