Department of Pharmacology, Brehm Center for Diabetes, University of Michigan Medical School, Ann Arbor, MI
Oxford Centre for Diabetes, Endocrinology & Metabolism, Radcliffe Department of Medicine, University of Oxford, Churchill Hospital, Oxford, U.K.
Diabetes. 2020 May;69(5):830-836. doi: 10.2337/dbi19-0012.
The coordinated electrical activity of β-cells within the pancreatic islet drives oscillatory insulin secretion. A recent hypothesis postulates that specially equipped "hub" or "leader" cells within the β-cell network drive islet oscillations and that electrically silencing or optically ablating these cells suppresses coordinated electrical activity (and thus insulin secretion) in the rest of the islet. In this Perspective, we discuss this hypothesis in relation to established principles of electrophysiological theory. We conclude that whereas electrical coupling between β-cells is sufficient for the propagation of excitation across the islet, there is no obvious electrophysiological mechanism that explains how hyperpolarizing a hub cell results in widespread inhibition of islet electrical activity and disruption of their coordination. Thus, intraislet diffusible factors should perhaps be considered as an alternate mechanism.
胰岛内β细胞的协调电活动驱动胰岛素的振荡分泌。最近的一个假设认为，胰岛内的β细胞网络中专门配备的“中枢”或“主导”细胞驱动胰岛的振荡，而电沉默或光消融这些细胞会抑制胰岛其余部分的协调电活动（从而抑制胰岛素分泌）。在这篇观点文章中，我们根据电生理学理论的既定原则讨论了这一假设。我们的结论是，虽然β细胞之间的电耦合足以使兴奋在胰岛中传播，但没有明显的电生理学机制可以解释为什么使中枢细胞超极化会导致胰岛电活动的广泛抑制以及破坏它们的协调性。因此，胰岛内的扩散因子可能应该被视为另一种机制。
