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.