Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. PCOS is a heterogeneous clinical condition, characterized by hirsutism, acne and/or androgenetic alopecia, irregular menstrual cycles and infertility. Moreover, a considerable percentage of PCOS women present insulin resistance, in particular those with obesity. The pathogenesis of the syndrome is still unclear, but neuroendocrine mechanisms have been studied in the last years. Although an inappropriate GnRH/LH secretion is well established, some obese and hyperinsulinemic women with PCOS present an attenuation of these neuroendocrine abnormalities. Recently, we described a negative correlation between leptin and LH levels in PCOS patients, suggesting that the attenuation in basal or stimulated response of LH in obese PCOS patients might be related to a leptin-resistant state. On the other hand, there is some evidence that the somatotrophic axis plays a role in the pathogenesis of PCOS. Recent data from our group showed a higher clonidine-induced GH secretion in normal weight and normoinsulinemic PCOS patients than in patients with idiopathic hirsutism. Thus, GH could act as a co-gonadotropic factor stimulating androgen production by the ovary or, alternatively, these results may just represent an epiphenomenon related to the high androgen levels and subsequent conversion to estrogens. Further studies are needed to elucidate the mechanisms related to data described in the present work and their relevance on the etiopathogenesis, diagnosis and treatment of PCOS.
Polycystic ovary syndrome; Hyperandrogenism; Insulin resistance; Somatotrophic axis; Luteinizing hormone; Leptin
