快樂小藥師 Im pharmacist nichts glücklich

Insulin Secretion and the α_2A-Adrenergic Receptor.

Rosengren and colleagues monitored the rate of fusion of insulin granules with the plasma membrane in pancreatic beta cells from rats that were either genetically susceptible or not susceptible to diabetes. The researchers went on to show that a comparatively small genetic locus in these rats was associated with increased production of α_2A-adrenergic receptors. Signaling from these receptors reduced the number of insulin vesicles docked at the membrane and hence the ability of the cells to release insulin. Pharmacologic inhibition of the α_2A-adrenergic receptors by yohimbine reversed the defective insulin release in diabetes-susceptible islets.