胰岛素诱导豚鼠卵母细胞减数分裂:与内源性黄体酮的关系

C. Lessman, A. Schuetz
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引用次数: 32

摘要

卵泡壁先前已被证明参与胰岛素诱导的红蛙卵泡卵母细胞成熟过程。在孕酮放射免疫测定法(RIA)的发展之后,研究了类固醇参与胰岛素诱导成熟的研究,以测量与体外培养相关的内源性孕酮。胰岛素和蛙垂体匀浆(FPH)均能显著提高孕酮水平。FPH对黄体酮水平的升高比胰岛素更有效,使黄体酮的升高比胰岛素大2个数量级。去除卵泡壁消除了胰岛素的类固醇效应。在完整卵泡中,观察到胰岛素诱导卵母细胞生发囊泡破裂(GVBD)的能力有相当大的动物间差异。有人提出,内源性黄体酮的差异可能解释了这种差异。为了验证这一假设,进行了一项实验,在同一动物的卵泡中同时测定激素分泌和卵泡对胰岛素的敏感性。实验结果表明,胰岛素诱导GVBD的能力,如50%应答所需的有效浓度(ED50),与RIA测量的内源性孕酮水平密切相关。结果提供了直接的证据,证明胰岛素对卵泡壁的作用涉及类固醇的产生。由此得出结论,内源性孕酮的增加促进了胰岛素诱导的GVBD。目前尚不清楚这两种激素如何相互作用以产生增强的效果,但可能涉及受体或受体后水平的相互作用。这个卵泡系统可能为这两种重要激素的作用模式和相互作用提供重要的见解。
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Insulin induction of meiosis of rana pipiens oocytes: Relation to endogenous progesterone
The follicle wall was previously shown to be involved in insulin induction of oocyte maturation in Rana pipiens ovarian follicles. Steroidogenic involvement in insulin induction of maturation was investigated following development of a radioimmunoassay (RIA) for progesterone to measure endogenous progesterone associated with in vitro incubates. Insulin and frog pituitary homogenate (FPH) were both found to elevate progesterone levels significantly in these incubates. FPH was more effective in elevating progesterone levels than insulin and caused progesterone increase of about 2 orders of magnitude greater than insulin. Removal of the follicle wall eliminated the steroidogenic effects of insulin. Considerable interanimal variation was observed in the ability of insulin to induce oocyte germinal vesicle breakdown (GVBD) in intact follicles. The hypothesis was proposed that differences in endogenous progesterone might explain this variation. To test this hypothesis, an experiment was carried out in which hormone production and follicular sensitivity to insulin were simultaneously determined in follicles obtained from the same animals. Results of the experiment show that the ability of insulin to induce GVBD, as indicated by the effective concentration needed for 50% response (ED50), was strongly correlated with the levels of endogenous progesterone as measured by RIA. The results provide direct evidence that insulin's action on the follicle wall involves steroid production. It was thus concluded that increased endogenous progesterone facilitates GVBD induction by insulin. It is unclear how the two hormones interact to produce an enhanced effect, but interactions at the receptor or postreceptor level may be involved. This follicle system may provide important insights into the mode of action and interaction of these two important hormones.
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