Stimulation of glucose transport in rat adipocytes by calcium

Abstract

Glucose transport in rat adipocytes was studied by monitoring the conversion of [1-14C]-glucose to 14CO2 in a system where glucose transport was made rate-limiting by increasing the flux through the pentose phosphate pathway with phenazine methosulphate, an agent which rapidly reoxidizes NADPH. Calcium increased both basal and insulin-stimulated apparent rates of glucose transport by approximately 40%. The maximum velocity of the apparent rate of glucose transport was increased by extracellular calcium both in the presence or absence of insulin. There was no change in the glucose concentration required for half-maximal rates of 14CO2 production. Calcium also enhanced the stimulation of apparent rates of glucose transport by insulin when examined over a range of hormone concentrations. Adipocyte cAMP concentrations were significantly lowered by calcium under conditions which led to increased apparent rates of glucose transport. In contrast, cobalt and nickel, antagonists of calcium action, elevated adipocyte cAMP levels and inhibited apparent rates of glucose transport. Agents which inhibit transmembrane calcium flux (verapamil, tetracaine, and procaine) inhibited apparent rates of glucose transport despite a reduction in adipocyte cAMP concentration.On the basis of the above data we suggest that calcium may increase apparent rates of glucose transport in rat adipocytes both by lowering intracellular cAMP concentration and by a further mechanism independent of changes in the level of cAMP. These results are consistent with the hypothesis that glucose transport in rat adipocytes may be controlled, in part, by a cAMP-induced phosphorylation mechanism.