Pancreatic islets exhibit bursting oscillations in response to elevated blood glucose. These oscillations are accompanied by oscillations in the free cytosolic Ca2+ concentration (Cac ), which drives pulses of insulin secretion. Both islet Ca2+ and metabolism oscillate, but there is some debate about their interrelationship. Recent experimental data show that metabolic oscillations in some cases persist after the addition of diazoxide (Dz), which opens K(ATP) channels, hyperpolarizing β-cells and preventing Ca2+ entry and Ca2+ oscillations. Further, in some islets in which metabolic oscillations were eliminated with Dz, increasing the cytosolic Ca2+ concentration by the addition of KCl could restart the metabolic oscillations. Here we address why metabolic oscillations persist in some islets but not others, and why raising Cac restarts oscillations in some islets but not others. We answer these questions using the dual oscillator model (DOM) for pancreatic islets. The DOM can reproduce the experimental data and shows that the model supports two different mechanisms for slow metabolic oscillations, one that requires calcium oscillations and one that does not.

中文翻译：

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胰岛中的钙和代谢振荡：谁在驾驶巴士？*


胰岛因血糖升高而表现出爆发性振荡。这些振荡伴随着游离胞质 Ca2+ 浓度 (Cac) 的振荡，从而驱动胰岛素分泌脉冲。胰岛 Ca2+ 和新陈代谢都会振荡，但关于它们之间的相互关系存在一些争议。最近的实验数据表明，在某些情况下，添加二氮嗪 (Dz) 后代谢振荡会持续存在，二氮嗪 (Dz) 打开 K(ATP) 通道，使 β 细胞超极化并阻止 Ca2+ 进入和 Ca2+ 振荡。此外，在一些用 Dz 消除代谢振荡的胰岛中，通过添加 KCl 增加胞质 Ca2+ 浓度可以重新启动代谢振荡。在这里，我们解释了为什么代谢振荡在某些胰岛中持续存在，而在其他胰岛中不存在，以及为什么提高 Cac 会在某些胰岛中重新启动振荡，而在其他胰岛中则不会。我们使用胰岛双振荡器模型 (DOM) 回答这些问题。 DOM 可以重现实验数据，并表明该模型支持两种不同的缓慢代谢振荡机制，一种需要钙振荡，另一种则不需要。