Research Progress on Pathogenesis of Obesity-Induced Insulin Resistance and Its Therapeutic Targets: PPARα/γ

Zhigang      Qi; Meilin      Xie

Abstract

Insulin resistance (IR) is defined as a decreased response of peripheral tissues to insulin. It is a common cause of cardiovascular and hepatic diseases, and often precedes the onset of hyperglycemia and predicts the development of type 2 diabetes. Free fatty acids (FFA), inflammation and oxidative stress play key roles in the development and/or progression of IR induced by obesity. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily; PPAR agonists can improve IR by regulating glucose and lipid metabolisms, and by inhibiting inflammatory and oxidative stress responses. In the article, we will review the pathogenesis of obesity-induced IR, its therapeutic targets: PPARα/γ, and discuss the signal transduction pathways through which these drugs exert therapeutic effects.

Keywords: obesity, insulin resistance, PPARα/γ