Kelly J J, Rajkovic I A, O'Sullivan A J, Sernia C, Ho K K
Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, Australia.
Clin Endocrinol (Oxf). 1993 Nov;39(5):561-7. doi: 10.1111/j.1365-2265.1993.tb02410.x.
Insulin like growth factor-I (IGF-I) levels in post-menopausal women are reduced by oral administration of the synthetic oestrogen ethinyl oestradiol but increased by transdermal delivery of 17 beta-oestradiol. Since these oestrogen types are different, the aim of this study was to clarify whether reduction in IGF-I is a specific effect of ethinyl oestradiol or common to other oral oestrogen formulations.
Randomized cross-over study comparing one month of treatment with ethinyl oestradiol (20 micrograms), conjugated equine oestrogen (1.25 mg Premarin) and oestradiol valerate (2 mg).
Six healthy post-menopausal women, age 60.3 +/- 5.6 years.
Mean 24 hour GH (from hourly sampling), IGF-I, GH binding protein (GHBP), pituitary (LH, FSH) and hepatic function (SHBG and angiotensinogen) were measured.
All three oestrogen formulations resulted in a significant reduction in IGF-I levels compared to baseline and significant elevations of GH and GHBP (P < 0.05). The percentage increase in GH during oestrogen treatment was significantly related to the percentage decrease in IGF-I levels (P = 0.04). All three oestrogen formulations resulted in significant suppression of LH and FSH and induction of the hepatic proteins, SHBG and angiotensinogen (P < 0.05). GHBP increased in parallel with other hepatic proteins.
Reduction in IGF-I levels is an intrinsic effect of oral oestrogen therapy and increased GH levels may occur as a result of reduced feedback inhibition by IGF-I. Since GHBP activity is not changed by transdermal oestrogen, we conclude that the liver is a major source of circulating GHBP and that GHBP is an oestrogen sensitive protein.
口服合成雌激素炔雌醇可降低绝经后女性的胰岛素样生长因子-I(IGF-I)水平,而经皮递送17β-雌二醇则可使其升高。由于这些雌激素类型不同,本研究的目的是阐明IGF-I的降低是炔雌醇的特异性作用还是其他口服雌激素制剂的共同作用。
随机交叉研究,比较炔雌醇(20微克)、结合马雌激素(1.25毫克倍美力)和戊酸雌二醇(2毫克)治疗1个月的效果。
6名健康绝经后女性,年龄60.3±5.6岁。
测量24小时平均生长激素(每小时采样)、IGF-I、生长激素结合蛋白(GHBP)、垂体功能(促黄体生成素、促卵泡生成素)和肝功能(性激素结合球蛋白和血管紧张素原)。
与基线相比,所有三种雌激素制剂均导致IGF-I水平显著降低,生长激素和GHBP显著升高(P<0.05)。雌激素治疗期间生长激素的百分比增加与IGF-I水平的百分比降低显著相关(P=0.04)。所有三种雌激素制剂均导致促黄体生成素和促卵泡生成素显著抑制以及肝脏蛋白性激素结合球蛋白和血管紧张素原的诱导(P<0.05)。GHBP与其他肝脏蛋白平行增加。
IGF-I水平降低是口服雌激素治疗的内在作用,生长激素水平升高可能是由于IGF-I反馈抑制降低所致。由于经皮雌激素不会改变GHBP活性,我们得出结论,肝脏是循环GHBP的主要来源,且GHBP是一种雌激素敏感蛋白。