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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.
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