Genetic Markers of Polycystic Ovary Syndrome: Emphasis on Insulin Resistance

Figure 2

The vicious cycle between hyperinsulinemia and hyperandrogenemia underlying PCOS development: compensatory hyperinsulinemia expands the androgen pool by acting directly on the thecal ovarian cells and indirectly by reducing hepatic biosynthesis of SHBG and IGFBP-1. Excess androgens in turn stimulate VAT to generate FFAs which further contributes to insulin resistance. These phenomena work hand in hand to maintain the PCOS state. SHBG: sex hormone binding globulin; IGFBP-1: insulin-like growth factor binding protein 1; VAT: visceral adipose tissue; FFAs: free fatty acids; LH: luteinizing hormone.