Abnormal GnRH pulsatility in polycystic ovary syndrome: Recent insights

Abstract

Although the fundamental symptoms of polycystic ovary syndrome (PCOS) relate most directly to ovarian dysfunction, central neuroendocrine systems play a prominent role in its pathophysiology. Gonadotropin-releasing hormone (GnRH) pulse generator resistance to negative feedback contributes to rapid GnRH pulse secretion, which promotes gonadotropin abnormalities that foster ovarian hyperandrogenemia and ovulatory dysfunction. The causes of GnRH neuron dysfunction, however, have remained enigmatic. In this review, we highlight a number of recent preclinical and clinical studies pertinent to the neuroendocrine abnormalities of PCOS, including those that have provided important insights into the relevance of animal models with PCOS-like features, the potential roles of kisspeptin and γ-aminobutyric acid (GABA)-ergic neurons, and the potential role of anti-Müllerian hormone.