The dual regulation of calcium efflux from pancreatic islets.
Calcium fluxes in islet cells were investigated by monitoring the efflux of 45Ca from prelabelled and perifused rat pancreatic islets. Glucose 16.7 mM provokes an initial fall followed 3 to 4 minutes later by a dramatic increase in 45Ca efflux. Both movements represent sustained phenomena which can be masked by one another. They both depend on the integrity of glucose metabolism and are also observed in response to other nutrients such as glyceraldehyde and alpha-keto-isocaproate. The secondary rise, which only occurs in the presence of extracellular calcium is thought to correspond to a Ca-Ca exchange mechanism and hence to reflect an increase in the rate of 40Ca influx. The initial fall in 45Ca efflux depends on the presence of extracellular sodium. Manipulation of the extracellular sodium concentration indicates the existence in islet cells of a glucose-sensitive Na-Ca counter transport process conceivably responsible for active extrusion of calcium. Inhibition of such a process appears to be the mechanism by which glucose initially reduced 45Ca efflux. By both decreasing the exit and increasing the entry of calcium into the beta-cell, glucose may provoke a sufficient intracellular accumulation of calcium to trigger insulin release.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D005947:Glucose / Q000502:physiology*; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism
D007328:Insulin; D012964:Sodium; D005947:Glucose; D002118:Calcium