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pubmed:abstractText |
D-Glucose catabolism was examined in rat pancreatic islets and tumoral insulin-producing cells (RINm5F line) exposed to D-[5-3H]glucose, D-[3,4-14C]glucose or D-[6-14C]glucose. In normal islets, a rise in D-glucose concentration from 2.8 to 16.7 mM augmented (i) the transfer of NADH, presumably via the glycerol phosphate shuttle, into the mitochondria, (ii) the decarboxylation of pyruvate and (iii) the oxidation of acetyl residues, even when the flow rates were expressed relative to the total rate of D-glucose utilization. Islet cells are thus organized to favour those mitochondrial oxidative events yielding the major fraction of the energy derived from the catabolism of D-glucose. In tumoral islet cells of the RINm5F line, all three oxidative mitochondrial processes, when expressed relative to the overall rate of D-glucose utilization, occurred at a low rate and failed to increase in response to the rise in D-glucose concentration. These findings emphasize the importance of distal regulatory processes in the control of D-glucose catabolism in normal islet cells, and document the perturbation of such processes in a model of dysfunction for this fuel-sensor organ.
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