It has been reported that insulin resistance and consequent hyperinsulinemia play a prominent role in hyperandrogenemia through direct way, induction of androgen production by theca cells, and indirect ways like elevation of luteinizing hormone (LH) secretion, decreasing insulin-like growth factor (IGF) binding protein, and reducing hepatic synthesis of sex hormone binding globulin (SHBG) and consequently free androgen level augmentation occurs (4-6). This evidence concerns the gene SHBG and polycystic ovary syndrome.