By deﬁnition obesity implies an excess of adipose tissue, which is not an inert storage room for triglycerides but actually the largest hormonally active gland of the body (1). Fat cells are known to convert androstenedione to estrone (2,3). Increased concentrations of estrone in obesity may interfere with the feedback system to the hypothalmohypophysial axis, increasing the levels of gonadotropins and androgens (4). As a consequence anovulation may occur. Furthermore, in obesity a reduction in sex hormone-binding globulin (SHBG) concentrations is seen, and the end result is an increased concentration of biologically active free androgens.