Lebrun P, van Ganse E, Juvent M, Deleers M, Herchuelz A
Biochim Biophys Acta. 1986 May 29;886(3):448-56. doi: 10.1016/0167-4889(86)90181-3.
The effect of amiloride, an inhibitor of Na+-H+ exchange, on intracellular pH (pHi), 86Rb outflow, 45Ca outflow and insulin release from pancreatic rat islets was examined. In the 0.1-1 mM range, amiloride transiently reduced pHi of glucose-deprived islets and allowed glucose to induce a sustained decrease in pHi of the islet cells. Amiloride reproduced the effect of glucose to decrease 86Rb and 45Ca outflow. In the presence of glucose (5.6 mM or more), amiloride (100 microM) acted synergistically with the sugar to reduce K+ outflow, and to stimulate 40Ca inflow and insulin release from perifused islets. These results add strong support to the view that the generation of protons through the metabolism of glucose represents an important step in the process of glucose-induced release. The stimulation by glucose of Na+-H+ exchange apparently masks and even overcomes the glucose-induced decrease in pHi otherwise expected from the increase in catabolic fluxes.
研究了钠氢交换抑制剂氨氯吡咪对大鼠胰岛细胞内pH值（pHi）、⁸⁶Rb外流、⁴⁵Ca外流及胰岛素释放的影响。在0.1 - 1 mM范围内，氨氯吡咪可短暂降低无糖培养胰岛的pHi，并使葡萄糖诱导胰岛细胞的pHi持续下降。氨氯吡咪重现了葡萄糖降低⁸⁶Rb和⁴⁵Ca外流的作用。在有葡萄糖（5.6 mM或更高）存在时，氨氯吡咪（100 μM）与葡萄糖协同作用，减少钾外流，并刺激钙内流及从灌流胰岛释放胰岛素。这些结果有力地支持了这样一种观点，即通过葡萄糖代谢产生质子是葡萄糖诱导释放过程中的一个重要步骤。葡萄糖对钠氢交换的刺激作用显然掩盖甚至克服了因分解代谢通量增加本应出现的葡萄糖诱导的pHi降低。
