2-Deoxy-D-glucose, not mercaptoacetate, induces a reversible reduction of body temperature in male desert hamsters (Phodopus roborovskii).

The initiation of torpor is supposed to be related to the availability of metabolic fuels. Studies on metabolic fuel inhibition of glucose by using 2-deoxy-D-glucose (2DG) or fatty acid by mercaptoacetate (MA) in heterothermic mammals produced mixed outcomes. To examine the roles of availability of glucose and fatty acid in the initiation of torpor in desert hamsters (Phodopus roborovskii), we intraperitoneally administrated 2DG and MA to summer-acclimated male hamsters while body temperature (T), metabolic rate (MR) and respiratory quotient (RQ) were simultaneously recorded to monitor their thermoregulatory response. 2DG induced a reversible reduction of T in desert hamsters both at ambient temperature (T) of 23°C and 5°C. At T of 23°C, T, MR and RQ decreased in a dose-dependent manner with a large T-T differential (> 6.5°C) and a lowest T of 28.0°C which were comparable to those in fasted hamsters. At T of 5°C, 2DG-treated hamsters also decreased T to the same level as at T 23°C, but MR was significantly higher than that at T of 23°C at each dose, suggesting doses of 2DG directly affected the hypothalamic T set-point. Different from fasted hamsters which maintain normothermic at T of 5°C, 2DG-treated hamsters showed a substantial reduction of T at T 5°C, indicting an overwhelming effect on the thermoregulatory system regardless of T. Furthermore, the rapid decrease of T and outstretched body posture in 2DG-treated hamsters suggest that the effects of 2DG were not simply mimicking the torpor pathways but that other mechanisms are involved. Interestingly, MA failed to induce a torpor-like state in male desert hamsters. Our results suggest that availability of glucose rather than fatty acid plays an important role for initiation of torpor in desert hamsters.