Giudice Linda C
Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, 505 Parnassus Avenue, M1496, Box 0132, San Francisco, CA 94143-0132, USA.
Best Pract Res Clin Endocrinol Metab. 2006 Jun;20(2):235-44. doi: 10.1016/j.beem.2006.03.005.
Polycystic ovarian syndrome (PCOS) is a common endocrinopathy characterized by oligo/anovulatiaon and elevated circulating androgens or evidence of hyperandrogenism after all known potential causes have been excluded. In addition, insulin resistance and accompanying hyperinsulinemia commonly occur in women with PCOS. There is increasing evidence that the endocrinologic and metabolic abnormalities in PCOS may have complex effects on the endometrium, contributing to the infertility and endometrial disorders observed in women with this syndrome. Androgen receptors and steroid receptor co-activators are over-expressed in the endometrium of women with PCOS. Also, biomarkers of endometrial receptivity to embryonic implantation-such as alpha(v)beta3-integrin and glycodelin-are decreased, and epithelial expression of estrogen receptor alpha (ERalpha) abnormally persists in the window of implantation in endometrium in women with PCOS. In addition to being responsive to the steroid hormones estradiol, progesterone, and androgens, the endometrium is also a target for insulin, the receptor for which is cyclically regulated in normo-ovulatory women. In vitro, insulin inhibits the normal process of endometrial stromal differentiation (decidualization). In addition, insulin-like growth factors (IGFs) and their binding proteins are regulated in and act on endometrial cellular constituents, and hyperinsulinemia down-regulates hepatic IGFBP-1, resulting in elevated free IGF-I in the circulation. Thus, elevated estrogen (without the opposing effects of progesterone in the absence of ovulation), hyperinsulinemia, elevated free IGF-I and androgens, and obesity all likely contribute to endometrial dysfunction, infertility, increased miscarriage rate, endometrial hyperplasia, and endometrial cancer common in women with PCOS. The potential mechanisms underlying these disorders, specifically in women with PCOS, are complex and await additional transdisciplinary research for their complete elucidation.
多囊卵巢综合征（PCOS）是一种常见的内分泌疾病，其特征为排卵稀少/无排卵以及循环雄激素升高，或在排除所有已知潜在病因后存在高雄激素血症的证据。此外，胰岛素抵抗及伴随的高胰岛素血症在PCOS女性中普遍存在。越来越多的证据表明，PCOS中的内分泌和代谢异常可能对子宫内膜产生复杂影响，导致该综合征女性出现不孕和子宫内膜疾病。雄激素受体和类固醇受体共激活因子在PCOS女性的子宫内膜中过度表达。此外，子宫内膜对胚胎着床的接受性生物标志物，如α（v）β3整合素和糖蛋白140减少，且雌激素受体α（ERα）在PCOS女性子宫内膜的着床窗期上皮表达异常持续存在。子宫内膜不仅对甾体激素雌二醇、孕酮和雄激素有反应，也是胰岛素的作用靶点，在正常排卵女性中其受体受到周期性调节。在体外，胰岛素会抑制子宫内膜基质分化（蜕膜化）的正常过程。此外，胰岛素样生长因子（IGFs）及其结合蛋白在子宫内膜细胞成分中受到调节并发挥作用，高胰岛素血症会下调肝脏IGFBP - 1，导致循环中游离IGF - I升高。因此，雌激素升高（在无排卵情况下缺乏孕酮的拮抗作用）、高胰岛素血症、游离IGF - I和雄激素升高以及肥胖都可能导致PCOS女性常见的子宫内膜功能障碍、不孕、流产率增加、子宫内膜增生和子宫内膜癌。这些疾病潜在的机制，特别是在PCOS女性中，很复杂，有待更多跨学科研究来全面阐明。
