Henquin J C
I Physiologisches Institut, University of Saarland, Homburg/Saar, FRG.
Biochem Biophys Res Commun. 1988 Oct 31;156(2):769-75. doi: 10.1016/s0006-291x(88)80910-0.
Tolbutamide and diazoxide, which respectively decrease and increase the activity of ATP-sensitive K+ channels, were used to investigate whether these channels play a role in the control of glucose-induced electrical activity (slow waves with spikes) in pancreatic B-cells. Addition of tolbutamide to a medium containing 10 mM glucose largely mimicked the effects of a rise in glucose concentration from 10 to 15 mM on electrical activity, ionic fluxes and insulin release. Tolbutamide was still active in the presence of maximally effective concentrations of glucose (30-40 mM). Diazoxide restored slow waves of membrane potential in B-cells which were persistently depolarized by 30 mM glucose. It is concluded that ATP-sensitive K+ channels are still operative at high glucose concentrations. These channels could thus be one target on which physiological concentrations of glucose act to regulate electrical activity in B-cells and, hence, insulin release.
甲苯磺丁脲和二氮嗪分别降低和增加ATP敏感性钾通道的活性，被用于研究这些通道是否在胰腺β细胞中葡萄糖诱导的电活动（伴有锋电位的慢波）的调控中发挥作用。向含有10 mM葡萄糖的培养基中添加甲苯磺丁脲，在很大程度上模拟了葡萄糖浓度从10 mM升高到15 mM对电活动、离子通量和胰岛素释放的影响。在存在最大有效浓度葡萄糖（30 - 40 mM）的情况下，甲苯磺丁脲仍然具有活性。二氮嗪恢复了被30 mM葡萄糖持续去极化的β细胞膜电位的慢波。得出的结论是，ATP敏感性钾通道在高葡萄糖浓度下仍起作用。因此，这些通道可能是生理浓度的葡萄糖作用于调控β细胞电活动从而调控胰岛素释放的一个靶点。
