Resistance of the insulinotropic action of alpha-D-glucose and beta-L-glucose pentaacetates to cholera and pertussis toxins.

The pentaacetate esters of alpha-D-glucose and beta-L-glucose were recently reported to stimulate insulin release. The possible participation of G-protein-coupled receptors to the insulinotropic action of these esters was investigated in rat pancreatic islets either preincubated with cholera toxin or obtained from animals injected with pertussis toxin. Neither procedure affected adversely the secretory response to the esters in islets incubated in the presence of L-leucine. Thus, in both situations, alpha-D-glucose pentaacetate and, to a lesser extent, beta-L-glucose pentaacetate augmented insulin release evoked by the branched-chain amino acid, whilst beta-L-galactose pentaacetate failed to do so. These findings suggest that G-proteins sensitive to either cholera or pertussis toxins are not involved in one of the two modalities by which these esters are thought to stimulate insulin secretion, namely that independent of the catabolic fate of their hexose moieties.