Insulin sensitivity and polycystic ovarian syndrome

Insulinresistance, commonly associated with polycystic ovarian syndrome (PC OS), raises many unresolved debates about its prevalence, mechanism and tru e pathological role. Low insulin sensibility may have multiple origins amon g them genetic molecular defects in pathways of cellular insulin effects. A weight gain and android distribution of fat mass may reveal or increase in sulin resistance and hyperinsulinemia. The preexisting unbalanced ovarian s teroidogenesis secondary to abnormalities in gene coding for enzymes of P45 0C17 alpha might be the necessary support facilitating the stimulatory effe ct of hyperinsulinemia or other factors (LH, IGF1) on ovarian androgens. In practice, the phycisian has to know how to evaluate and to treat insulin r esistance in view of its implication in dysovulation and, later on, metabol ic and cardiovascular risks. Nutritional education and regular physical exe rcice are the necessary approaches. The efficacy and indications of metform in and thiazolidinediones have to be further evaluated.