par Malaisse, Willy 
;Hutton, J C;Sener, Abdullah ;Levy, J.;Herchuelz, André ;Devis, Ghislain;Somers, G
Référence The journal of membrane biology, 38, 3, page (193-208), 002
Publication Publié, 1978-01
;Hutton, J C;Sener, Abdullah ;Levy, J.;Herchuelz, André ;Devis, Ghislain;Somers, GRéférence The journal of membrane biology, 38, 3, page (193-208), 002
Publication Publié, 1978-01
Article révisé par les pairs
| Résumé : | 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. |
