Ishihara S, Taketani Y, Mizuno M
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Japan.
Endocrinol Jpn. 1988 Oct;35(5):691-6. doi: 10.1507/endocrj1954.35.691.
The effect of estradiol on glycogen synthesis was examined in a primary cell culture system of the human endometrium. Estradiol inhibited glycogen synthesis in a dose dependent manner with a minimum effective dose of 10(-9)M. Progesterone-induced glycogen synthesis was completely abolished by the simultaneous addition of estradiol. Estradiol did not affect the activity of glycogen phosphorylase in endometrial cells, but the activity of glycogen synthetase was decreased by estradiol irrespective of the presence of progesterone. The inhibitory effect of estradiol on the glycogen synthesis of endometrial cells seemed to be mediated by estradiol receptor, because LY156758, an antiestrogenic drug at receptor site, reversed the inhibitory effect of estradiol.
在人子宫内膜原代细胞培养系统中研究了雌二醇对糖原合成的影响。雌二醇以剂量依赖方式抑制糖原合成，最小有效剂量为10(-9)M。同时添加雌二醇可完全消除孕酮诱导的糖原合成。雌二醇不影响子宫内膜细胞中糖原磷酸化酶的活性，但无论孕酮是否存在，雌二醇均可降低糖原合成酶的活性。雌二醇对子宫内膜细胞糖原合成的抑制作用似乎是由雌二醇受体介导的，因为受体位点的抗雌激素药物LY156758可逆转雌二醇的抑制作用。
