McCartney Christopher R, Campbell Rebecca E
Center for Research in Reproduction and Department of Medicine, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Centre for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand 9054.
Curr Opin Endocr Metab Res. 2020 Jun;12:78-84. doi: 10.1016/j.coemr.2020.04.005. Epub 2020 Apr 23.
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.
尽管多囊卵巢综合征（PCOS）的基本症状与卵巢功能障碍最为直接相关，但中枢神经内分泌系统在其病理生理学中起着重要作用。促性腺激素释放激素（GnRH）脉冲发生器对负反馈的抵抗导致GnRH脉冲快速分泌，这会促使促性腺激素异常，进而导致卵巢雄激素过多血症和排卵功能障碍。然而，GnRH神经元功能障碍的原因仍然不明。在本综述中，我们重点介绍了一些与PCOS神经内分泌异常相关的近期临床前和临床研究，包括那些对具有PCOS样特征的动物模型的相关性、亲吻素和γ-氨基丁酸（GABA）能神经元的潜在作用以及抗苗勒管激素的潜在作用提供了重要见解的研究。
