IR appears to contribute to hyperandrogenism and other gonadotropin abnormalities through two mechanisms: 1)a hyperinsulinemic state reduces circulating sex hormone binding globulin (SHBG) levels, causing an increase in bioavailable (free) testosterone since less SHBG is available to bind with testosterone; 2) high insulin concentrations stimulate androgen biosynthesis through ovaries (14, 17): insulin decreases Insulin Growth Factor binding globulin 1 (IGFBP-1) and increases free IGF and thus increases ovarian theca cell proliferation and androgenesis as well. This evidence concerns the gene SHBG and hyperandrogenism.