The existing evidence suggests that androgen excess favors abdominal visceral adiposity, and visceral fat encourages further production of androgens through the direct effect of several mediators including hypoadiponectinemia, increased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and leptin levels and other factors, or as a result of insulin resistance and hyperinsulinims [25]. Here, LEP is linked to Insulin resistance.