Abstract

PCOS is one of the most frequent endocrine diseases in women. It was initially described as a reproductive disease. However, growing data have shown a strong association with metabolic dysfunction. Ovulatory dysfunction and Metabolic Syndrome are more frequently found in severe PCOS phenotypes. Insulin resistance and hyperandrogenemia are critical factors in PCOS pathophysiology and are strongly interrelated. A vicious circle where hyperandrogenism favors abdominal fat accumulation and insulin resistance has been described in PCOS. Furthermore, IR reciprocally facilitates the hypersecretion of androgens in PCOS patients. In the last years, several mechanisms responsible for follicular growth arrest has been described. Extraovarian mechanism of follicle arrest demonstrates a crucial role of inheriting or acquired insulin resistance, because of abdominal fat accumulation can induce or worsen hyperandrogenism in PCOS. Hyperandrogenism and HI can cause an impairment of FSH and LH secretion leading to follicle arrest. The improvement of the MS by weight loss or medical treatment can restore follicle growth ovulation in some PCOS phenotypes, but not in all of them.