HEXOSE METABOLISM IN PANCREATIC-ISLETS - REGULATION OF AEROBIC GLYCOLYSIS AND PYRUVATE DECARBOXYLATION

1. D-Glucose (0.5-16.7 mM) preferentially stimulates aerobic glycolysis and D-[3,4-C-14]glucose oxidation, relative to D-[5-H-3]glucose utilization in rat pancreatic islets, the concentration dependency of such a preferential effect displaying a sigmoidal pattern. 2. Inorganic and organic calcium antagonists, as well as Ca2+ deprivation, only cause a minor decrease in the ratio between D-[3,4-C-14]glucose oxidation and D-[5-H-3]glucose utilization in islets exposed to a high concentration of the hexose (16.7 mM). 3. Non-glucidic nutrient secretagogues such as 2-aminobicyclo[2,2,1]heptane-2-carboxylate (BCH), 2-ketoisocaproate and 3-phenylpyruvate fail to stimulate aerobic glycolysis and D-[3,4-C-14]glucose oxidation in islets exposed to 6.0 mM D-glucose. Nevertheless, BCH augments [1-C-14]pyruvate and [2-C-14]pyruvate oxidation. 4. The glucose-induced increment in the paired ratio between D-[3,4-C-14]glucose oxidation and D-[5-H-3]glucose utilization is impaired in the presence of either cycloheximide or ouabain. 5. These findings suggest that the preferential effect Of D-glucose upon aerobic glycolysis and pyruvate decarboxylation is not attributable solely to a Ca2+-induced activation of FAD-linked glycerophosphate dehydrogenase and/or pyruvate dehydrogenase, but may also involve an ATP-modulated regulatory process.