卵巢类固醇生成的局部控制

PhD Helen Mason (Senior Research Fellow), MD, FRCP, Hon MD(Uppsala) Stephen Franks (Professor of Reproductive Endocrinology)
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引用次数: 16

摘要

许多假定的旁分泌因子现在被认为与FSH相互作用,控制卵巢类固醇生成。这些因素的相对重要性仍有待确定,但胰岛素样生长因子及其结合蛋白的存在,以及后者通过局部产生蛋白酶来控制的机制,表明该系统在卵泡形成中起作用。我们已经证明了多囊卵巢妇女组织中类固醇激素的过量产生。单层培养的卵泡膜细胞产生过量的黄体酮和雄烯二酮,颗粒细胞的雌二醇产生明显增强,以响应FSH。最近的证据表明,类固醇激素表达或翻译中的遗传缺陷是雄激素过量产生的原因,但涉及的基因或基因尚未确定。我们小组的数据表明,来自无排卵多囊卵巢的颗粒细胞过早成熟,我们假设这是由于这些卵泡中循环胰岛素水平升高与LH的相互作用,这种相互作用导致卵泡生长受阻。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
4 Local control of ovarian steroidogenesis

A number of putative paracrine factors are now thought to interact with FSH in the control of ovarian steroidogenesis. The relative importance of these factors remains to be determined, but the presence of the insulin-like growth factors and their binding proteins and the mechanism of control of the latter through the local production of proteases suggests a role for this system in folliculogenesis.

We have demonstrated over-production of steroid hormones in tissue from women with polycystic ovaries. Theca cells in monolayer culture produced excessive amounts of progesterone and androstenedione and granulosa cell oestradiol production was considerably enhanced in response to FSH. Recent evidence points to a genetic defect in the expression or translation of steroidogenic hormones as a cause of excess androgen production, but the gene or genes involved has not been established. Data from our group suggest that granulosa cells from anovulatory polycystic ovaries are prematurely matured and we hypothesize that this is due to the interaction of the raised circulating insulin levels with LH in these follicles, an interaction that results in arrested follicular growth.

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