In general, the effects of insulin resistance and subsequent hyperinsulinemia on ovarian function are thought to occur as follows: insulin promotes androgen secretion through luteinizing hormone (LH) stimulation to increase the number of initial antral follicles by increasing free androgen via decreased sex hormone-binding globulin (SHBG), which leads to follicular atresia as a result of continuously high androgen levels [5]. This evidence concerns the gene SHBG and Insulin resistance.