Glycolysis in the mouse uterus during the early post-implantation stages of pregnancy and the effects of acute doses of ethanol.

The objective of this study was to assess the possibility that, in mice, alcohol interferes with uterine glycolysis to influence indirectly embryonal development. Glycolysis was found to be a major metabolic process in the mouse uterus and its pattern of activity changed during post-implantation pregnancy between days 5 and 9. This was evidenced by changes in glycolytic enzymes and intermediates, and in the capacity of endometrial preparations to consume oxygen and produce lactate during incubation in vitro. The intraperitoneal administration of ethanol at 3.0 and 6.0 gm/kg body weight, but not at 1.5 gm/kg body weight, on day 9 of pregnancy modified glycolysis in the uterus after 2 hours, resulting in significant changes in the rates of accumulation of glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, and citrate. These effects were not mediated by changes in redox state, since the ratio of lactate to pyruvate remained unchanged after injection of ethanol. Citrate was considered to be a major factor involved both in the regulation of uterine glycolysis and in the ethanol-induced alterations in the levels of hexose phosphates. The elevated levels of uterine glucose registered after treatment with ethanol were related to an acceleration of glycogen degradation in the liver and not in the uterine endometrium. The results suggest that part of the adverse action that these doses of ethanol exert on embryonal development stems from indirect effects that involve uterine functions relating to the nurture of the conceptus via glycolysis.