Cataldo N A
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, USA.
Semin Reprod Endocrinol. 1997 May;15(2):123-36. doi: 10.1055/s-2007-1016295.
Insulin-like growth factor (IGF) binding proteins are produced by ovarian follicular cells and can oppose the effects of the IGFs and gonadotropins on these cells. Since polycystic ovarian syndrome (PCOS) is characterized by disordered follicular development, with the accumulation of antral follicles within the ovary which fail to respond appropriately to endogenous FSH, it has been hypothesized that one or more IGFBPs, which can act as FSH antagonists in vitro, could play a role in inhibiting follicular development in this syndrome. Follicular fluid IGFBP levels, however, do not differ between PCOS follicles and the androgenic, presumably atretic follicles of cycling women without PCOS. Serum IGFBP-1 levels are lower in PCOS, likely because of hyperinsulinemia, and serum free IGF-1 levels are raised. This alternation may drive the excess thecal androgen production characteristic of PCOS follicles. Alterations in IGFBPs may sustain the anovulatory steady state in PCOS but are unlikely to initiate development of the syndrome.
胰岛素样生长因子(IGF)结合蛋白由卵巢卵泡细胞产生,可对抗IGF和促性腺激素对这些细胞的作用。由于多囊卵巢综合征(PCOS)的特征是卵泡发育紊乱,卵巢内窦卵泡积聚,对内源性促卵泡生成素(FSH)反应异常,因此有人推测,一种或多种在体外可作为FSH拮抗剂的IGF结合蛋白可能在该综合征中抑制卵泡发育。然而,PCOS卵泡与无PCOS的周期正常女性的雄激素化、可能闭锁的卵泡之间,卵泡液IGF结合蛋白水平并无差异。PCOS患者血清IGFBP-1水平较低,可能是由于高胰岛素血症,而血清游离IGF-1水平升高。这种改变可能导致PCOS卵泡特征性的过量卵泡膜雄激素生成。IGF结合蛋白的改变可能维持PCOS的无排卵稳态,但不太可能引发该综合征的发生。