Calcium antagonists and islet function: VII. Effect of calcium deprivation.
The role of extracellular Ca2+ in the regulation of islet function is investigated. Decreasing extracellular Ca2+ concentrations cause a dose-related inhibition of glucose-induced insulin release. Whereas the efflux of 45Ca from perifused islets is transiently increased on exposure to Ca2+-deprived media, it is unaffected by a partial lowering of the extracellular Ca2+ concentration. Under the latter condition, therefore, the observed reduction in the size of the islets' exchangeable calcium pool(s) appears to be due to reduced Ca2+ entry. The proper effect of glucose on Ca handling by the islets is apparently not affected by a lowering in the extracellular Ca2+ concentration. Nevertheless, in islets exposed to glucose and incubated in Ca2+-deprived media, glucose uptake and oxidation and lactate output are decreased, whereas the islet ATP level is increased, as if extracellular Ca2+ shortage were to affect not only the cellular pool of Ca regulating insulin release, but also energy-consuming processes possibly located at the cell membrane.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D008274:Magnesium / Q000494:pharmacology; D051381:Rats
D007328:Insulin; D007773:Lactates; D000255:Adenosine Triphosphate; D008274:Magnesium; D005947:Glucose; D002118:Calcium