Poretsky L, Piper B
Department of Medicine, Cabrini Medical Center, New York, New York.
Obstet Gynecol. 1994 Oct;84(4):613-21.
To review the literature dealing with the roles of insulin resistance and elevated LH levels in the development of the polycystic ovary syndrome and to outline a new hypothesis of the pathogenesis of this disorder.
We reviewed articles on the topics of insulin resistance, elevated LH levels, and polycystic ovary syndrome that were contained in the CD-PLUS MEDLINE system data base for years 1976-1994.
Ninety-one original reports published in English-language, peer-reviewed biomedical journals were selected.
The selected studies were reviewed critically and their conclusions were evaluated. The available literature indicates that insulin resistance and increased LH secretion are frequent features of polycystic ovary syndrome and may be important in its pathogenesis. It appears that both the amplitude and the frequency of LH pulses are increased in this disorder. Although the causes of these abnormalities of LH secretion are unknown, they could be either primary (due to increased sensitivity of LH secretion to GnRH) or secondary (due to the effects of sex steroids on LH secretion). The cause of insulin resistance in polycystic ovary syndrome also is unknown. It most likely results from a post-binding defect in the insulin action pathway. There is both in vitro and in vivo evidence that elevated LH and hyperinsulinemia act synergistically to enhance ovarian growth, androgen secretion, and ovarian cyst formation.
Based on the available literature, we propose a "dual-defect" hypothesis of polycystic ovary syndrome. We suggest that in a significant subset of patients, this disorder may be caused by a conjunction of two independent genetic defects: one that produces elevated LH secretion and another that produces insulin resistance. Thus, polycystic ovary syndrome develops as a result of the synergistic action of increased LH levels and hyperinsulinemia on the ovary. This working hypothesis may serve as a useful guide for further studies of the pathogenesis of polycystic ovary syndrome.
回顾有关胰岛素抵抗和促黄体生成素（LH）水平升高在多囊卵巢综合征发病中作用的文献，并概述该疾病发病机制的新假说。
我们查阅了1976 - 1994年CD - PLUS MEDLINE系统数据库中有关胰岛素抵抗、LH水平升高和多囊卵巢综合征主题的文章。
选取91篇发表于英文、经同行评审的生物医学期刊上的原始报告。
对所选研究进行严格审查并评估其结论。现有文献表明，胰岛素抵抗和LH分泌增加是多囊卵巢综合征的常见特征，可能在其发病机制中起重要作用。在该疾病中，LH脉冲的幅度和频率似乎均增加。尽管这些LH分泌异常的原因尚不清楚，但可能是原发性的（由于LH分泌对促性腺激素释放激素（GnRH）的敏感性增加）或继发性的（由于性类固醇对LH分泌的影响）。多囊卵巢综合征中胰岛素抵抗的原因也尚不清楚。它很可能是由胰岛素作用途径中的结合后缺陷导致的。体外和体内均有证据表明，LH升高和高胰岛素血症协同作用可促进卵巢生长、雄激素分泌和卵巢囊肿形成。
基于现有文献，我们提出多囊卵巢综合征的“双缺陷”假说。我们认为，在相当一部分患者中，该疾病可能由两个独立的基因缺陷共同导致：一个导致LH分泌升高，另一个导致胰岛素抵抗。因此，多囊卵巢综合征是由于LH水平升高和高胰岛素血症对卵巢的协同作用而发展形成的。这一工作假说可为进一步研究多囊卵巢综合征的发病机制提供有用的指导。
