Misler S, Barnett D W, Falke L C
Department of Medicine (Jewish Hospital), Washington University, Saint Louis, Missouri 63130.
Pflugers Arch. 1992 Jun;421(2-3):289-91. doi: 10.1007/BF00374842.
Sodium azide (NaN3), a reversible inhibitor of mitochondrial respiration, blocks glucose-induced electrical activity and insulin secretion in human pancreatic islet B cells. Here we show that brief (10-15 min) application followed by removal of 3 mM NaN3 results in transient overshoot of electrical activity and insulin secretion even at substimulatory levels of glucose (3-5 mM). In addition, application of NaN3, even at very low [Ca2+]o, reversibly increases cytosolic Ca2+ to levels usually associated with substantial insulin release. These results suggest that (i) metabolic inhibition may reset B cell stimulus-secretion coupling and (ii) a rise in free cytosolic Ca2+, by itself, is not sufficient to trigger insulin secretion.
叠氮化钠（NaN₃）是一种线粒体呼吸的可逆抑制剂，可阻断人胰岛B细胞中葡萄糖诱导的电活动和胰岛素分泌。我们在此表明，短暂（10 - 15分钟）应用3 mM叠氮化钠后再去除，即使在亚刺激水平的葡萄糖（3 - 5 mM）下，也会导致电活动和胰岛素分泌的短暂超调。此外，即使在非常低的细胞外钙离子浓度（[Ca²⁺]ₒ）下应用叠氮化钠，也会使细胞质钙离子可逆地增加到通常与大量胰岛素释放相关的水平。这些结果表明：（i）代谢抑制可能会重置B细胞刺激-分泌偶联；（ii）细胞质游离钙离子的升高本身不足以触发胰岛素分泌。
