LAUSR

Abstract Objective Elevated intracellular cAMP concentrations potentiate insulin secretion from pancreatic β cells. Phosphodiesterase 3B (PDE3B) is highly expressed in these cells and plays a role in the regulation of insulin secretion. Materials and methods In this study, effects of amrinone, an inhibitor of PDE3B on insulin release from isolated pancreatic islets, were determined. Results Exposure of islets to amrinone for 15, 30 and 90 min markedly increased secretion induced by 6.7 mM glucose. Amrinone enhanced also secretion stimulated by 6.7 mM glucose and DB-cAMP, an activator of PKA. It was also demonstrated that amrinone potentiated insulin secretion induced by 6.7 mM glucose in the combination with PMA (activator of PKC) or acetylcholine. However, the insulin-secretory response to glucose and glibenclamide was unchanged by amrinone. Conclusions These results indicate that amrinone is capable of increasing insulin secretion; however, its action is restricted.