ABSTRACT
Peroxisome proliferator-activated receptor gamma (PPAR ) is a member of a subfamily of nuclear receptor transcription factors with primary roles in fat metabolism. PPAR is expressed most abundantly not only in adipose tissue adipocytes and macrophages, but also in muscle and liver and to lesser degrees in other tissues (1). The thiazolidinediones (TZDs) are synthetic agonists of PPAR . Thiazolidinediones act primarily in adipose tissue, where they have regenerative, lipometabolic, endocrine, and anti-inflammatory effects. These effects directly and indirectly promote insulin-mediated glucose uptake in muscle and fat, insulin-mediated suppression of hepatic glucose production (2), and pancreatic insulin secretion (3). Clinically, the increase in insulin sensitivity promotes lower glucose levels in people with diabetes, impaired fasting glucose (IFG), and impaired glucose tolerance (IGT). To date, the TZDs that have been used to treat diabetes include pioglitazone, rosiglitazone, and troglitazone. Of these, troglitazone was removed from the market due to idiosyncratic liver toxicity (not seen with the other two).
