Effect of low temperatures on glucoseinduced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat

The direct effect of cold on the inhibition of B cell secretion is well known in hibernating and experimen-tally hypothermic mammals. This temperature depen-dency may result from the inhibition of ion transport across the membranes. In order to verify this hypothe-sis, ionic effluxes and insulin secretion from rat islets loaded with 86Rb+ and 45Ca2+ were measured during perifusion. At 37 \s=deg\C,the rise in glucose concentration from zero to 16\m=.\7mmol/l provoked a rapid decrease in 86Rb+ efflux, an early fall and subsequent rise in 45Ca2+ efflux and a typical biphasic pattern of insulin secretion. At 27 \s=deg\C,glucose induced only a very slight increase in insulin secretion, while the fluxes of radioactive ions were not significantly modified in amplitude but were clearly delayed. At 17 \s=deg\C,no insu-lin response to glucose was observed and the decrease in K+ conductance indicated by 86Rb+ flux decrease was less temperature-dependent than the movement of Ca2+. After supplementary stimulation with a high extracellular concentration of Ca2+, insulin secretion was enhanced at 27 \s=deg\Cand reached levels induced by glucose alone at 37 \s=deg\C.An increase in hormone secretion occurred even at 17 \s=deg\C,but only during a first phase of secretion. Regular increases in temperature potentiated insu-lin secretion and provoked changes in ionic fluxes which suggest that B cell depolarization (86Rb+ flux decrease) induced by glucose can occur at 15 \s=deg\Cbut cannot induce the opening of voltage-dependent Ca2+ channels (increase in 45Ca2+ efflux) until tempera-tures higher than 27 \s=deg\Care reached. These results suggest that cooling affects calcium movements especially rather than K+ conductance and insulin exocytosis per se