Siegel E G, Wollheim C B, Sharp G W, Herberg L, Renold A E
Biochem J. 1979 Apr 15;180(1):233-6. doi: 10.1042/bj1800233.
In pancreatic islets from normal Chinese hamsters preloaded with 45Ca2+, glucose-induced biphasic insulin release was associated with increased 45Ca2+ efflux; islets from diabetic hamsters showed decreased insulin release and no increase in 45Ca2+ efflux. The lack of stimulated 45Ca2+ efflux persisted even when glucose-induced insulin release was potentiated by 3-isobutyl-1-methylxanthine. Since glucose-stimulated 45Ca2+ uptake by diabetic islets was not impaired, a defect in intracellular Ca2+ handling may be involved in the defective insulin release of the diabetic Chinese hamster.
在预先加载了45Ca2+的正常中国仓鼠胰岛中，葡萄糖诱导的双相胰岛素释放与45Ca2+外流增加有关；糖尿病仓鼠的胰岛胰岛素释放减少，45Ca2+外流没有增加。即使3-异丁基-1-甲基黄嘌呤增强了葡萄糖诱导的胰岛素释放，受刺激的45Ca2+外流缺乏的情况仍然存在。由于糖尿病胰岛对葡萄糖刺激的45Ca2+摄取没有受损，细胞内Ca2+处理缺陷可能与糖尿病中国仓鼠胰岛素释放缺陷有关。
