The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non‐fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol‐induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT ‐2.58°C, COLD: ‐5.08°C). Ethanol produced significant dose‐dependent elevations in blood glucose levels over the 4‐hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/ kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common gene
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