Jijakli H, Malaisse W J
Laboratory of Experimental Medicine, Erasmus School of Medicine, Brussels Free University, Belgium.
Cell Signal. 1997 May-Jun;9(3-4):283-90. doi: 10.1016/s0898-6568(96)00183-0.
Pancreatic islets prelabelled with either 86Rb or 45Ca were exposed to a rise in D-glucose concentration from 2.8 to 16.7 mM whilst perifused in the presence of 2 microM glibenclamide, 30 mM extracellular K+ and both 30 mM K+ and 250 microM diazoxide. In all three situations, the rise in glucose concentration provoked a dramatic increase in insulin output, despite unchanged or even increased efflux of 86Rb from the prelabelled islets. Also in all three situations, glucose sharply decreased effluent radioactivity from islets prelabelled with 45Ca but perifused in the absence of extracellular Ca2+, while augmenting 45Ca efflux, to a variable extent, from islets perifused at normal extracellular Ca2+ concentration (1.0 mM). It is proposed, therefore, that the insulinotropic action of D-glucose in depolarized islets, and presumably also under normal conditions, may involve the gating of voltage-insensitive Ca2+ channels.
预先用⁸⁶Rb或⁴⁵Ca标记的胰岛,在2微摩尔格列本脲、30毫摩尔细胞外K⁺以及30毫摩尔K⁺和250微摩尔二氮嗪存在的情况下进行灌流时,使其D - 葡萄糖浓度从2.8毫摩尔升至16.7毫摩尔。在所有这三种情况下,尽管预先标记的胰岛中⁸⁶Rb的流出量未变甚至增加,但葡萄糖浓度的升高仍引发了胰岛素分泌的显著增加。同样在所有这三种情况下,葡萄糖使预先用⁴⁵Ca标记但在无细胞外Ca²⁺情况下灌流的胰岛流出放射性急剧降低,而在正常细胞外Ca²⁺浓度(1.0毫摩尔)灌流的胰岛中,葡萄糖在不同程度上增加了⁴⁵Ca的流出。因此,有人提出,D - 葡萄糖在去极化胰岛中的促胰岛素作用,大概在正常情况下也是如此,可能涉及对电压不敏感的Ca²⁺通道的开启。