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

Figure 2

PPARγ and AT2R implications in PCOS-associated defects. PPARγ (and maybe AT2R) agonists increase tyrosine phosphorylation of IRS-1. Insulin-stimulated androgen production has been shown to be increased by specific inhibition of MEK. MEK/ERK activity was found to be constitutively reduced in PCOS women, inhibited by NEFAs, and activated by PPARγ agonists. AT2R activation counteracts lipotoxic effects of NEFA either directly or through activation of PPARγ. Adapted from [10].