Calcium movements and insulin release in pancreatic islet cells.
The mechanisms by which glucose provokes the intracellular accumulation of calcium in the B-cell were investigated by monitoring the efflux of 45Ca from preloaded and perifused rat pancreatic islets. Glucose provoked an initial fall followed by a secondary rise in 45Ca efflux. These two movements are sustained and reversible. They display distinct sensitivities towards glucose but both movements depend on the integrity of glucose metabolism in the islets. The secondary rise in 45Ca efflux reflects the rate of calcium influx through voltage-sensitive calcium channels and corresponds to a process of calcium-calcium exchange. Glucose gates the calcium channels by increasing the endogenous generation of reduced pyridine nucleotides. The absence of extracellular sodium reduced the efflux of 45Ca and the inhibitory effect of glucose on calcium outflow. This suggests the existence in the islets of a process of sodium-calcium countertransport responsible for calcium extrusion from the B-cell. Glucose reduces 45Ca efflux by inhibiting this process. This inhibition may result from an increased endogenous generation of protons. In conclusion, glucose provokes an intracellular accumulation of calcium within the B-cell both by gating voltage-sensitive calcium channels and by inhibiting sodium-calcium countertransport.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007473:Ion Channels / Q000187:drug effects; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D009249:NADP / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism
D007328:Insulin; D007473:Ion Channels; D009249:NADP; D012964:Sodium; D005947:Glucose; D002118:Calcium