Since fish are poikilothermic, changes in temperature may perturb hormonal activation of cell function. To test this hypothesis, and determine the extent to which hormonal responses are thermally compensated, the effect of temperature on epinephrine-stimulated glucose release in perfused trout liver was studied. Thermally acclimated (5 and 20°C) rainbow trout (Oncorhynchus mykiss) were responsive to epinephrine (0.5×10-6 mol l-1) at both 5 and 20°C. Metoprolol (beta2 antagonist) and propranolol (beta1and2) decreased the response significantly (to 1.4 % and 8.4 % of stimulated values, respectively) while phentolamine (alpha1and2) was without effect, implying the response is beta2-mediated. Both basal (86 and 19 micromole g-1 liver h-1 in 5 and 20°C trout, respectively) and epinephrine-stimulated (210 and 168 micromole g-1 h-1) rates of glucose release were higher (2.4-fold higher for epinephrine-stimulated and 8.8-fold for basal) in 5°C- than in 20°C-acclimated fish, regardless of perfusion temperature. Although the dose-response curve for epinephrine was markedly temperature-dependent, cold- and warm-acclimated fish were affected in different ways. Cold-acclimated fish (5°C) were less responsive to epinephrine when perfused at 5°C (ED50 6.8×10-9 mol l-1) than when perfused at 20°C (ED50 8.2×10-10 mol l-1); in contrast, warm-acclimated fish (20°C) were less responsive to epinephrine when perfused at 20°C (ED50 4.6×10-7 mol l-1) than at 5°C (ED50 6.6×10-9 mol l-1). These results are interpreted as being indicative of adaptations to maintain the capacity for hepatic glucose mobilization at low temperature.

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