Considering female infertility, hyperinsulinemia has been shown to contribute to hyperandrogenism and anovulation by mechanisms involving ovarian and adrenal androgen synthesis, and synergistically with LH, promoting the growth and formation of ovarian cysts by making them hyperresponsive to growth hormone, without allowing the selection and maturity of a single follicle and the corresponding ovulation (37). This evidence concerns the gene GH1 and hyperandrogenism.