Glucoprivation induces anestrus and lipoprivation may induce hibernation in Syrian hamsters.

Previous results supported the notion that estrous cycles in Syrian hamsters are responsive to the general availability of metabolic fuels, rather than to either fatty acid or glucose availability per se. To test this idea, we monitored estrous cycles in hamsters that were fed ad libitum and treated with a range of doses of 2-deoxy-D-glucose (2-DG), an inhibitor of glucose utilization. Hamsters treated with 2-DG at doses ranging from 750-1,250 mg/kg showed normal estrous cycles, but higher doses (1,750 or 2,000 mg/kg) induced anestrus. While it is clear from these data that estrous cycles are affected by glucoprivation, it is not clear whether they are responsive to decreased fatty acid availability. Groups of hamsters were fed ad libitum and treated with a range of doses of methyl palmoxirate (MP), an inhibitor of fatty acid utilization. Some of the hamsters that received the highest doses became torpid and thus were not tested for lordosis. None of the euthermic, MP-treated hamsters became anestrous. Other experiments examined the role of glucose availability in fasted hamsters. Hamsters with a high body fat content were protected from fasting-induced anestrus. In contrast, fat food-deprived hamsters treated with low doses of 2-DG (750 mg/kg) became anestrous. Thus fatty acids mobilized from adipose tissue did not prevent fasting-induced anestrus when glucose utilization was blocked. One interpretation is that during fasting fatty acid utilization spares glucose for other tissues involved in the control of estrous cycles.(ABSTRACT TRUNCATED AT 250 WORDS)