Functional hyperandrogenism is a common endocrinological disorder of premenopausal wo­men characterized by hyperandrogenism, hirsutism with or without androgenic alopecia and chronic anovulation. The controversy regarding the pathophysiological mechanism underl­ying the disease still persists. Insulin resistance and hyperinsulinism are now well recognized features of obese women with functional hyperandrogenism and accepted pathogenetic fac­tor of disorder in obese patients. Insulin enhances lutheotropic hormone secretion and together with it promotes synthesis of androgens in ovaries. Insulin affects the degree of free andro­gens by lowering serum concentrations of sex-hormone binding globuline. It stimulates synthesis of androgens in adrenal glands and ovaries by enhancing activity of citocrom P450c17alpha.

Non-obese women with functional hyperandrogenism have less expressed insulin resi­stance and higher serum growth hormone concentrations than obese androgenized women as well as weight matched controls. Higher growth hormone directly and indirectly (through insulin-like growth factor-I) influence ovarian cells and stimulates androgen synthesis. The­re is possible link between both known aethiopathogenetic factors of functional hyperandrogenism: growth hormone induces insulin resistance and hyperinsulinaemia, which in turn sensitate peripheral tissues for growth hormone.