Central vs. peripheral metabolic control of estrous cycles in Syrian hamsters. II. Glucoprivation

Estrous cycles in Syrian hamsters are inhibited by food deprivation or treatment with pharmacological inhibitors of intracellular glucose utilization (glucoprivic treatments). These same metabolic challenges increase neural stimulation in areas of the caudal brain stem thought to be involved in detection of metabolic signals. Experiment 1 was designed to examine whether vagally transmitted signals are important for glucoprivic effects on estrous cycles and on neural stimulation in the caudal brain stem. Vagotomized or sham-operated hamsters were treated with 2-deoxy-D-glucose (2-DG) at a dose known to decrease cellular glucose utilization and inhibit estrous cycles (1,750 mg/kg). Vagotomized and sham-operated hamsters did not differ significantly in incidence of 2-DG-induced anestrus or in neural stimulation in the caudal brain stem, but the effects of 2-DG on estrous cycles and neural stimulation appeared to have been attenuated in vagotomized hamsters. In experiment 2, hamsters were injected intracerebroventricularly with 2-DG or glucose at doses that did not induce anestrus when injected systemically (125 and 250 mg/kg). Groups treated with intracerebroventricular injections of 2-DG showed a significantly higher incidence of anestrus than those treated with glucose. In experiment 3, effects of systemic injections of 2-DG were prevented by prior injection of glucose or fructose at the same concentration, indicating that 2-DG acts via effects on glucose metabolism, rather than via a nonspecific pharmacological effect or generalized stress response. Results of these experiments and those reported elsewhere (J. E. Schneider, A. J. Hall, and G. N. Wade. Am. J. Physiol. 272 (Regulatory Integrative Comp. Physiol, 41) R400-R405, 1997] are consistent with the notion that central glucoprivation is sufficient, whereas peripheral lipoprivation is not critical, for metabolic effects on estrous cycles.