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The pancreatic β-cell plays a key role in glucose homeostasis by secreting insulin, the only hormone capable of lowering the blood glucose concentration. Impaired insulin secretion results in the chronic hyperglycemia that characterizes type 2 diabetes (T2DM), which currently afflicts >450 million people worldwide. The healthy β-cell acts as a glucose sensor matching its output to the circulating glucose concentration. It does so via metabolically induced changes in electrical activity, which culminate in an increase in the cytoplasmic Ca2+ concentration and initiation of Ca2+-dependent exocytosis of insulin-containing secretory granules. Here, we review recent advances in our understanding of the β-cell transcriptome, electrical activity, and insulin exocytosis. We highlight salient differences between mouse and human β-cells, provide models of how the different ion channels contribute to their electrical activity and insulin secretion, and conclude by discussing how these processes become perturbed in T2DM.

Original publication

DOI

10.1152/physrev.00008.2017

Type

Journal article

Journal

Physiol Rev

Publication Date

01/01/2018

Volume

98

Pages

117 - 214

Keywords

Animals, Calcium Channels, Diabetes Mellitus, Type 2, Exocytosis, Homeostasis, Humans, Insulin, Insulin-Secreting Cells, Mice