Herchuelz A, Thonnart N, Sener A, Malaisse W J
Endocrinology. 1980 Aug;107(2):491-7. doi: 10.1210/endo-107-2-491.
The effect of K+-induced depolarization on calcium fluxes and insulin release from isolated islets were investigated in order to elucidate the mechanism by which glucose initially reduces and later increases 45Ca efflux from prelabeled and perifused rat pancreatic islets. Raising the extracellular K+ concentration from 5.0 to 20.0 mM produced a 2- to 3-fold increase in 45Ca net uptake and efflux from isolated islets. The latter effect was dependent on the presence of extracellular Ca2+, suggesting that it resulted from the entry of calcium into the islet cells. In the presence of 20 mM K+, 16.7 mM glucose failed to stimulate 45Ca efflux, while 20 mM K+ further enhanced 45Ca efflux from islets perifused in the presence of the high concentration of glucose. These findings suggest that the effect of glucose to stimulate 45Ca efflux from perifused islets depends mainly on the glucose-induced depolarization of the cell membrane. In the absence of extracellular calcium, 20 mM K+ failed to mimick the effect of glucose to reduce 45Ca efflux. Glucose (16.7 mM) decreased 45Ca efflux from islets perifused in the presence of 20 mM K+ and antagonized the effect of 20 mM K+ to stimulate 45Ca efflux from perifused islets. It is concluded that K+-induced plasma membrane depolarization reproduces the effect of glucose to stimulate but not to inhibit 45Ca efflux from perifused islets.
为了阐明葡萄糖最初降低并随后增加预先标记并进行灌流的大鼠胰岛中45Ca流出的机制，研究了钾离子诱导的去极化对分离胰岛中钙通量和胰岛素释放的影响。将细胞外钾离子浓度从5.0 mM提高到20.0 mM，使分离胰岛中45Ca的净摄取和流出增加了2至3倍。后一种效应依赖于细胞外钙离子的存在，表明它是由钙离子进入胰岛细胞所致。在存在20 mM钾离子的情况下，16.7 mM葡萄糖未能刺激45Ca流出，而20 mM钾离子进一步增强了在高浓度葡萄糖存在下灌流的胰岛的45Ca流出。这些发现表明，葡萄糖刺激灌流胰岛中45Ca流出的效应主要取决于葡萄糖诱导的细胞膜去极化。在没有细胞外钙的情况下，20 mM钾离子未能模拟葡萄糖降低45Ca流出的效应。葡萄糖（16.7 mM）降低了在20 mM钾离子存在下灌流的胰岛的45Ca流出，并拮抗了20 mM钾离子刺激灌流胰岛中45Ca流出的效应。得出的结论是，钾离子诱导的质膜去极化重现了葡萄糖刺激但不抑制灌流胰岛中45Ca流出的效应。
