Role of Lipotoxicity and Contribution of the Renin-Angiotensin System in the Development of Polycystic Ovary Syndrome

Figure 3

Whole-body and cellular mechanisms of PPAR effects. At the adipocyte level, activation of peroxisome proliferator-activated receptors (PPARγ) increases the transcription of genes that induce adipogenesis as well as lipoprotein lipase (LPL) activation, which promotes the uptake of triglycerides by adipocytes. At the level of nonadipose tissues, activation of PPARγ increases the transcription of genes that induce fatty acid (FA) oxidation and mitochondrial biogenesis, which decrease intracellular overload of FA and FA metabolites. A PPARγ-induced reduction of circulating levels of nonesterified FA (NEFA) and triglyceride-rich lipoprotein contributes to the decrease in NEFA uptake by nonadipose tissues and the overload of NEFAs in these tissues.