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Insulinotropic action of β-L-glucose pentaacetate

par Malaisse, Willy ;Best, Leonard;Herchuelz, André ;Hiriart, Marcia;Jijakli, Hassan ;Kadiata, Marcel ;Larrieta-Carasco, Elena;Laghmich, Aouatif ;Louchami, Karim ;Mercan, Dany ;Olivares Fontt, Elizabeth ;Sànchez-Soto, Carmen;Scruel, Olivier ;Sener, Abdullah ;Valverde, Isabel;Villanueva-Peñacarrillo, María Luisa;Viñambres, Concepción;Zawalich, Walter
Référence American journal of physiology: endocrinology and metabolism, 275, 6 38-6, page (E993-E1006)
Publication Publié, 1998

Article révisé par les pairs

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Résumé :

The metabolism of β-L-glucose pentaacetate and its interference with the catabolism of L-[U-14C]glutamine, [U-14C]palmitate, D-[U- 14C]glucose, and D-[5-3H]glucose were examined in rat pancreatic islets. Likewise, attention was paid to the effects of this ester on the biosynthesis of islet peptides, the release of insulin from incubated or perifused islets, the functional behavior of individual B cells examined in a reverse hemolytic plaque assay of insulin secretion, adenylate cyclase activity in a membrane- enriched islet subcellular fraction, cAMP production by intact islets, tritiated inositol phosphate production by islets preincubated with myo-[2- 3H]inositol, islet cell intracellular pH, 86Rb and 45Ca efflux from prelabeled perifused islets, and electrical activity in single isolated B cells. The results of these experiments were interpreted to indicate that the insulinotropic action of β-L-glucose pentaacetate is not attributable to any nutritional value of the ester but, instead, appears to result from a direct effect of the ester itself on a yet unidentified receptor system, resulting in a decrease in K+ conductance, plasma membrane depolarization, and induction of electrical activity.