INSULIN STIMULATES ANDROGEN ACCUMULATION IN INCUBATIONS OF OVARIAN STROMA OBTAINED FROM WOMEN WITH HYPERANDROGENISM
INSULIN STIMULATES ANDROGEN ACCUMULATION IN INCUBATIONS OF OVARIAN STROMA OBTAINED FROM WOMEN WITH HYPERANDROGENISM
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DOI：
10.1210/jcem-62-5-904
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发表时间：
1986-05-01
影响因子：
5.8
通讯作者：
RYAN, KJ
中科院分区：
文献类型：
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作者：
BARBIERI, RL;MAKRIS, A;RYAN, KJ
从4例高雄激素血症妇女和3例非高雄激素血症妇女的卵巢间质中，观察了胰岛素和胰岛素样生长因子(IGF)对卵巢雄激素产生的影响。在从所有四名雄激素增多症患者获得的间质孵育中，单独胰岛素(500 ng/ml)显著刺激雄烯二酮和睾酮的释放。单用黄体生成素(25 ng/ml)可显著刺激4例高雄激素患者中3例的吻合口中雄烯二酮的释放，而4例高雄激素患者中1例的间质中有睾酮的释放。在四名高雄激素患者中的三名患者的间质培养中，单独使用胰岛素(500 ng/ml)导致雄烯二酮和睾酮的释放显著高于单独使用促黄体生成素(25 ng/ml)。从四名高雄激素女性中的三名获得的间质组织孵育中，二氢睾酮被释放出可测量的数量。在所有三种可检测到双氢睾酮的情况下，单独使用胰岛素(500 ng/ml)，但不单独使用促黄体生成素(25 ng/ml)，可显著刺激双氢睾酮的释放。从三名非高雄激素、正常周期的女性获得的间质培养显示，雄烯二酮的释放水平很低，睾酮和双氢睾酮的释放可以忽略不计。单独使用胰岛素(500 ng/ml)和黄体生成素(25 ng/ml)并不能显著增加雄烯二酮的释放。胰岛素(500 ng/m l)加黄体生成素(25 ng/m l)显著促进两名非高雄激素妇女的间质中雄烯二酮的积累。一项胰岛素剂量-反应实验是使用从一名高雄激素女性身上获得的间质组织进行的。在本实验中，剂量为50 ng/ml的胰岛素与剂量为500 ng/ml的胰岛素在刺激雄烯二酮和睾酮释放方面的效果相同。除胰岛素外，IGF-I/生长抑素C(50 ng/ml)还可刺激雄烯二酮和睾酮的释放。松弛素(1微克/毫升)和增殖刺激活性(50毫微克/毫升)不能刺激雄烯二酮和睾酮的释放。这些研究表明，人卵巢间质可能是胰岛素和IGF-I的靶组织，而高胰岛素血症可能是导致卵巢高雄激素血症的重要因素。
The effects of insulin and insulin-like growth factors (IGFs) on ovarian androgen production were examined in ovarian stroma obtained from four women with hyperandrogenism and three women without hyperandrogenism. In incubations of stroma obtained from all four hyprandrogenic patients, insulin alone (500 ng/ml) significantly stimulated androstenedione and testosterone release. LH alone (25 ng/ml) significantly stimulated androstenedione release in incubations of stoma obtained from three of the four hyperandrogenic patients with testosterone release in incubations of stroma obtained from one of the four hyperandrogenic patients. In stromal incubations from three of the four hyperandrogenic patients, insulin alone (500 ng/ml) resulted in a significantly greater release of androstenedione and testosterone than did LH alone (25 ng/ml). Dihydrotestosterone was released in measurable quantities in incubations of stromal tissue obtained from three of the four hyperandrogenic women. In all three instances in which dihydrotestosterone was detectable, insulin alone (500 ng/ml), but not LH alone (25 ng/ml), significantly stimulated dihydrostestosterone release. Incubations of stroma obtained from three nonhyperandrogenic, normally cycling women demonstrated low levels of androstenedione release and negligible testosterone and dihydrotestosterone release. Insulin alone (500 ng/ml) and LH alone (25 ng/ml) produced no significant increase in androstenedione release. Insulin (500 ng/ml) plus LH (25 ng/ml) significantly stimulated androstenedione accumulation in stroma obtained from two of the nonhyperandrogenic women. One insulin dose-response experiment was performed using stromal tissue obtained from a hyperandrogenic woman. In this experiment, insulin, at a dose of 50 ng/ml, was as effective as insulin at a dose of 500 ng/ml in stimulating androstenedione and testosterone release. In addition to insulin, IGF-I/somatomedin C (50 ng/ml) stimulated androstenedione and testosterone release. Relaxin (1 .mu.g/ml) and multiplication-stimulating activity (50 ng/ml) did not stimulate androstenedione and testosterone release. These studies suggest that human ovarian stroma may be a target tissue for insulin and IGF-I, and that hyperinsulinemia may be an important factor contributing to ovarian hyperandrogenism.