国际生殖健康/计划生育 ›› 2021, Vol. 40 ›› Issue (1): 79-83.doi: 10.12280/gjszjk.20200249

• 综述 • 上一篇    下一篇

多囊卵巢综合征神经内分泌病因机制的研究进展

钱紫薇, 姚琦, 周阁, 任青玲, 胡荣魁()   

  1. 210023 南京中医药大学医学院·整合医学学院(钱紫薇,姚琦); 南京中医药大学附属医院/江苏省中医院生殖医学科(周阁),妇科(任青玲,胡荣魁)
  • 收稿日期:2020-05-09 出版日期:2021-01-15 发布日期:2021-01-21
  • 通讯作者: 胡荣魁 E-mail:xiangyu198110@163.com
  • 基金资助:
    国家自然科学基金(81704164);江苏省“333工程”培养资金资助项目(2016Ⅲ-3288);江苏省六大人才高峰项目(WSN-044);江苏省人口学会开放基金课题(JSPA2019016)

Advances in Neuroendocrine Mechanism of Polycystic Ovary Syndrome

QIAN Zi-wei, YAO Qi, ZHOU Ge, REN Qing-ling, HU Rong-kui()   

  1. School of Medicine and Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China (QIAN Zi-wei, YAO Qi); Department of Reproductive Medicine (ZHOU Ge), Department of Gynecology (REN Qing-ling, HU Rong-kui), Affiliated Hospital of Nanjing University of Chinese Medicine/Jiangsu Province Hospital of Chinese Medicine, Nanjing 210023, China
  • Received:2020-05-09 Published:2021-01-15 Online:2021-01-21
  • Contact: HU Rong-kui E-mail:xiangyu198110@163.com

摘要:

多囊卵巢综合征(PCOS)是女性常见的生殖内分泌疾病,PCOS的典型特征是高雄激素血症、排卵障碍和卵巢多囊样改变。高雄激素血症通常是由垂体黄体生成激素(LH)脉冲分泌增加所致。多数PCOS女性表现为血清LH水平升高,LH脉动分泌频率升高。LH脉动分泌频率异常升高反映了促性腺激素释放激素(GnRH)神经回路异常活跃,提示PCOS的病因或临床表型具有神经内分泌基础。PCOS临床前动物模型的一些研究已经证实了GnRH神经元及其上游传入神经回路的改变。发育过程中过量雄激素或抗苗勒管激素暴露的PCOS模型证实了GnRH神经元活性的增加,与Kisspeptinergic、GABAergic神经元刺激性支配GnRH神经元有关。就PCOS高频率GnRH/LH脉冲的病理临床表现及其神经网络调控机制进行了综述,探讨PCOS的神经内分泌起源。

关键词: 多囊卵巢综合征, 性腺甾类激素, 神经反馈, 促性腺素释放激素, 促黄体激素, Kisspeptin能神经元, GABA能神经元

Abstract:

Polycystic ovary syndrome (PCOS) is a highly prevalent reproductive endocrine disorder in women. PCOS is characterized by three clinical features of hyperandrogenism, ovulatory dysfunction and the polycystic appearance of the ovaries. Hyperandrogenemia is driven by the increased luteinizing hormone (LH) pulse secretion from the pituitary. Indeed, PCOS women display both the elevated mean level of LH and the elevated frequency of LH pulses. The abnormally high frequency of LH pulses reflects a hyperactive circuit of gonadotropin-releasing hormone (GnRH) neurons, which suggests a neuroendocrine basis to either the etiology or phenotype of PCOS. Several studies in preclinical animal models of PCOS have demonstrated the alterations in GnRH neurons and their upstream afferent neuronal circuits. The PCOS model of excessive androgen or Mulller′s hormone exposure during development confirmed the increased activity of GnRH neurons that is related to the stimulation of Kisspeptinergic and GABAergic neurons to control GnRH neurons. In this paper, we review the pathology of PCOS associated with high frequency GnRH/LH pulses and highlight about the involved neural networks, and then discuss the neuroendocrine origins of PCOS.

Key words: Polycystic ovary syndrome, Gonadal steroid hormones, Neurofeedback, Gonadotropin-releasing hormone, Luteinizing hormone, Kisspeptinergic neurons, GABAergic neurons