Proper glycemic control requires that numerous β-cells are coordinated to rapidly, but temporarily, secrete insulin after meals. This coordination integrates hundreds of β-cells within each islet into a functionally homogeneous unit. This homogeneity occurs despite the intrinsic heterogeneity of individual β-cells (1). Fine-tuning of this coordination is further required because of the cyclic oscillations that ionic, metabolic, and effector events undergo within each islet, as well as among the many islets of a pancreas. Together, these events ensure normal pulsatility of insulin secretion (2,3). Many mechanisms have evolved over time to achieve this coordination (1–4). One such mechanism is cell-to-cell coupling, the process by which contiguous cells exchange cytosolic molecules (Fig. 1) via channels made of connexin (Cx) proteins. These proteins concentrate at gap junction domains of the cell membrane (4).
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