Abstract
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 ofd-[5-3H]glucose,d-[3,4-14C]glucose,d-[6-14C]glucose andd-[2-14C]glucose. Starvation decreased the generation of3HOH fromd-[5-3H]glucose and the production of14CO2 from14C-labelledd-glucose, both at low and high hexose concentrations. In islets from starved and fed rats, a rise ind-glucose concentration preferentially stimulated oxidative glycolysis, pyruvate decarboxylation and acetyl residue oxidation, relative tod-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 to14CO2 than their C2. Starvation decreased oxidative glycolysis more severely than non-oxidative glycolysis, impaired the preferential stimulation ofd-[3,4-14C]glucose oxidation relative tod-[5-3H]glucose utilization as observed in response to a rise in hexose concentration, and lowered the ratio betweend-[6-14C]glucose oxidation and hexose utilization. It is proposed, therefore, that the short-term regulation of mitochondrial oxidative events byd-glucose is itself modulated in islet cells by the nutritional status.
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