HEXOSE METABOLISM IN PANCREATIC-ISLETS - OXIDATIVE RESPONSE TO D-GLUCOSE IN FED AND STARVED RATS

Islets from fed and 3-day-starved rats were incubated for 60 min in the presence of either 2.8 or 16.7 mM D-glucose, mixed with tracer amounts of D-[5-H-3]glucose, D-[3,4-C-14]glucose, D-[6-C-14]glucose and D-[2-C-14]glucose. Starvation decreased the generation of (HOH)-H-3 from D-[5-H-3]glucose and the production of (CO2)-C-14 from C-14-labelled D-glucose, both at low and high hexose concentrations. In islets from starved and fed rats, a rise in D-glucose concentration preferentially stimulated oxidative glycolysis, pyruvate decarboxylation and acetyl residue oxidation, relative to D-glucose utilization. At both low and high hexose concentrations and in both fed and starved rats, the decarboxylation of pyruvate exceeded the oxidation of glucose-derived acetyl residues, the C1 of such residues being more efficiently converted to (CO2)-C-14 than their C2. Starvation decreased oxidative glycolysis more severely than non-oxidative glycolysis, impaired the preferential stimulation of D-[3,4-C-14[glucose oxidation relative to D-[5-H-3]glucose utilization as observed in response to a rise in hexose concentration, and lowered the ratio between D-[6-C-14[glucose oxidation and hexose utilization. It is proposed, therefore, that the short-term regulation of mitochondrial oxidative events by D-glucose is itself modulated in islet cells by the nutritional status.