par Malaisse, Willy 
;Lebrun, Philippe
Référence Diabetes care, 13 Suppl 3, page (9-17)
Publication Publié, 1990-08
;Lebrun, Philippe Référence Diabetes care, 13 Suppl 3, page (9-17)
Publication Publié, 1990-08
Article révisé par les pairs
| Résumé : | The mechanisms responsible for the stimulation of insulin release from the pancreatic beta-cell by hypoglycemic sulfonylureas are reviewed herein. One hypothesis postulates that these agents act, at the level of the plasma membrane, by causing the closure of a class of K+ channels characterized by their sensitivity to ATP. This may lead to depolarization of the plasma membrane, gating of voltage-sensitive Ca2+ channels, increase in cytosolic Ca2+ activity, and activation of the effector system for insulin release. However, it is not evident that the closure of ATP-sensitive K+ channels accounts for effects of sulfonylureas such as inhibition of K+ inflow into the islet cells, increase in their Na+ content, or even stimulation of Ca2+ inflow and insulin release at physiological or higher concentrations of D-glucose. |
