The regulation by estradiol-17β of lactate and α-glycerophosphate production from glucose and glucose 6-phosphate was investigated in uteri of ovariectomized rats. Time-course studies revealed that a single i.m. injection of estradiol-17β (10 μg/100g) produced statistically significant increases in lactate and α-glycerophosphate formation at 4 hr which reached peak levels at 16 hr. Both lactate and α-glycerophosphate production were enhanced after estradiol treatment to more than 200 per cent of the control values whether expressed per uterus or per mg DNA. Activities were greater with glucose 6-phosphate as substrate than with glucose indicating that glucose phosphorylation is an important rate -limiting step in the estrogenic stimulation of uterine glycolysis. The estradiol-induced increases in lactate and α-glycerophosphate production were reduced significantly by two anti estrogenic agents, nafoxidine hydrochloride (U-11100A) (50 μg/100 g) and ethamoxytriphetol (MER-25) (5 mg/100 g) as well as by progesterone (5 mg/100 g). Additionally, the administration of two anti-uterotrophic agents, actinomycin (25 μg/100 g) and cycloheximide (70 μg/100 g), resulted in almost complete inhibition of the estradiol-induced increases in the production of uterine lactate and α-glycerophosphate. The results described in this communication, along with our previous data on the estrogenic induction of several carbohydrate-metabolizing enzymes, are consonant with the suggestion that the process of estradiol-stimulated glycolysis in uterine tissue entails an increased formation of certain specific proteins.
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