Insulinotropic action of beta-L-glucose pentaacetate

The metabolism of beta-L-glucose pentaacetate and its interference with the catabolism of L-[U-C-14]glutamine, [U-C-14]palmitate, D-[U-C-14]glucose, a nd D-[5-H-3]glucose were examined in rat pancreatic islets. Likewise, atten tion was paid to the effects of this ester on the biosynthesis of islet pep tides,the release of insulin from incubated or perifused islets, the functi onal behavior of individual B cells examined in a reverse hemolytic plaque assay of insulin secretion, adenylate cyclase activity in a membrane-enrich ed islet subcellular fraction, cAMP production by intact islets, tritiated inositol phosphate production by islets preincubated with myo-[2-H-3]inosit ol, islet cell intracellular pH, Rb-86 and Ca-45 efflux from prelabeled per ifused islets, and electrical activity in single isolated B cells. The resu lts of these experiments were interpreted to indicate that the insulinotrop ic action of beta-L-glucose pentaacetate is not attributable to any nutriti onal value of the ester but, instead, appears to result from a direct effec t 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.