Abnormal GnRH pulsatility in polycystic ovary syndrome: Recent insights. (June 2020)

• Record Type: Journal Article
• Authors: McCartney, Christopher R.; Campbell, Rebecca E.
• Is Part Of: Current opinion in endocrine and metabolic research. Volume 12(2020)
• Page Start: 78
• Page End: 84
• Publication Date: 2020-06
• Subjects: Polycystic ovary syndrome -- Gonadotropin-releasing hormone -- GnRH neuron -- GnRH pulse generator -- Luteinizing hormone -- Hyperandrogenemia -- Kisspeptin -- γ-Aminobutyric acid -- Anti-Müllerian hormone -- Animal models of PCOS; Endocrine glands -- Diseases -- Periodicals; Metabolism -- Disorders -- Periodicals; Endocrine System Diseases; Metabolic Diseases; Endocrine glands -- Diseases; Metabolism -- Disorders; Periodical; Electronic journals; Periodicals; Electronic journals; 616.4
• DOI: 10.1016/j.coemr.2020.04.005
• Languages: English
• ISSNs: 2451-9650

Abstract

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.