Hyperphagia and anovulation are both triggered by prior food deprivation or other treatments that decrease intracellular availability of metabolic fuels in most species studied. Syrian hamsters fail to show compensatory hyperphagia, but do show anestrus in response to these energetic challenges. In the present experiments, we examined food intake, plasma glucose levels, and estrous cyclicity in Syrian hamsters in response to 2,5-anhydro-D-mannitol (2,5-AM), a fructose analog that is thought to trigger eating in rats by depleting intracellular levels of ATP. In experiment 1, female estrous cycling hamsters were treated with 100, 200, 400, or 800 mg/kg 2,5-AM or the vehicle by intraperitoneal injection. Food intake was measured 1, 2, 4, 8, and 24 h after treatment. There were no statistically significant increases in food intake in response to any dose of 2,5-AM. In experiment 2, blood samples were drawn at 0, 1, 3, 5, 7, and 25 h after hamsters were treated with 0 or 400 mg/kg 2,5-AM. 2,5-AM treatment resulted in a mild but significant decrease in plasma glucose levels similar to those seen in 2,5-AM-treated rats, suggesting that 2,5-AM has similar effects on fuel metabolism in rats and hamsters. In experiment 3, hamsters received 2,5-AM, 2,5-AM plus the fatty acid oxidation inhibitor methyl palmoxirate, or vehicle every 6 h over the first 48 h of the estrous cycle and were tested for indexes of estrous cyclicity at the end of the cycle. All hamsters showed normal estrous cycles, regardless of treatment. If 2,5-AM has similar metabolic consequences in rats and hamsters, the present results suggest that decreased intracellular levels of ATP and mild hypoglycemia do not increase food intake or inhibit estrous cyclicity in Syrian hamsters.
Hourly analysis of cerebrospinal fluid glucose shows large diurnal fluctuations
