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Resistance of the insulinotropic action of α‐D‐glucose and β‐L‐glucose pentaacetates to cholera and pertussis toxins
Author(s) -
Malaisse Willy J.,
Ladriere Laurence
Publication year - 1998
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549800202202
Subject(s) - cholera toxin , hexose , pertussis toxin , pancreatic islets , medicine , insulin , receptor , endocrinology , chemistry , l glucose , toxin , galactose , secretion , biochemistry , biology , islet , g protein , enzyme
The pentaacetate esters of α‐D‐glucose and β‐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, α‐D‐glucose pentaacetate and, to a lesser extent, β‐L‐glucose pentaacetate augmented insulin release evoked by the branched‐chain amino acid, whilst β‐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.