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Effects of high extracellular K+ concentrations, diazoxide and/or Ca2+ deprivation upon D-glucose metabolism in pancreatic islets

par Malaisse, Willy ;Picton, Sally;Malaisse Lagae, Francine ;Sener, Abdullah
Référence Biochimica et biophysica acta. Molecular cell research, 1451, 2-3, page (255-262)
Publication Publié, 1999-09

Article révisé par les pairs

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Résumé :

A rise in D-glucose concentration may augment insulin release independently of changes in K+ conductance or Ca2+ influx in pancreatic islet cells, the insulinotropic action of the hexose remaining dependent on an increased generation of high-energy phosphates. In the present study, therefore, it was investigated to which extent the procedures currently used to assess the modalities of the secretory response to D-glucose independent of its effect on ATP-sensitive K+ channels and Ca2+ inflow may themselves affect the catabolism of the hexose in isolated rat pancreatic islets. A rise in the extracellular K+ concentration from 5 to 30 or 60 mM failed to significantly affect the metabolism of D-glucose. At 90 mM K+, however, the maximal velocity of the glycolytic flux was decreased and the apparent K(m) for D-glucose lowered, without an obvious alteration of the preferential stimulation of oxidative mitochondrial events in response to a rise in d- glucose concentration. Such a preferential stimulation was abolished, however, either by diazoxide at a low, but not high, K+ concentration or by Ca2+ deprivation, in the absence or presence of diazoxide, at a high K+ concentration. It is speculated that these metabolic changes may be attributable, in part at least, to an altered activity of key cytosolic (e.g. pyruvate kinase) and mitochondrial (e.g. FAD-linked glycerophosphate dehydrogenase) enzymes.