Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men

Author:

Rorsman Patrik1,Ashcroft Frances M.1

Affiliation:

1. Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom; Department of Neuroscience and Physiology, Metabolic Research Unit, Göteborg, Sweden; and Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom

Abstract

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.

Funder

Wellcome Trust

Wellecome Trust

EC | European Research Council (ERC)

Publisher

American Physiological Society

Subject

Physiology (medical),Molecular Biology,Physiology,General Medicine

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