INS and polycystic ovary syndrome: Such an outcome might be expected since insulin acts as a co-gonadotropin in ovarian follicles [41,42,90] to promote cell survival and proliferation through the activity of phosphoinositide 3-kinase (PI3-Kinase) and mitogen-activated protein kinase (MAPK), to stimulate theca cell androstenedione and testosterone production as substrate for granulosa cell aromatization in PCOS women [112], and to enhance ovarian inositol-mediated insulin and gonadotropin action (thus reducing ovarian insulin resistance), supporting FSH-driven estradiol release from granulosa cells [42,44].