• 1 January 1981
    • journal article
    • research article
    • Vol. 218  (2) , 318-323
Abstract
The antinociceptive potency of morphine as determined by tail-flick test was significantly decreased in streptozotocin (STZ)-induced diabetic mice and mice pretreated with hypertonic dextrose or fructose. STZ-induced diabetic rats and spontaneously diabetic mice were also significantly less sensitive to the antinociceptive effects of morphine in the tail-flick test. Hypoglycemic mice were significantly more sensitive to morphine. Insulin-reversal of dextrose- and STZ-induced diabetic hyperglycemia returned sensitivity to morphine-induced antinociception to control values. Pretreatment with hypertonic 3-O-methylglucose (a nonmetabolizable sugar) had no effect on morphine potency. The ability of morphine to inhibit phenylquinone-induced writhing was attenuated in STZ-induced diabetic mice. Mice receiving various pretreatments (STZ-induced diabetes, STZ-induced diabetes plus insulin, dextrose, fasting or fasting plus insulin) were subjected to analyses of their serum glucose levels serum insulin levels and brain glucose levels. Apparently only hyper- or hypoglycemia correlated (inversely) with changes in the potency of morphine. It is hypothesized that the diabetes induced hyperglycemia is responsible for selectively affecting the potency of morphine.