Paracrine regulation of insulin secretion
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REVIEW
Paracrine regulation of insulin secretion Mark O. Huising 1,2 Received: 5 May 2020 / Accepted: 28 May 2020 / Published online: 31 August 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Pancreatic beta cells are the only cell type in our body capable of producing and secreting insulin to instruct the insulin-sensitive cells and tissues of our bodies to absorb nutrients after a meal. Accurate control of insulin release is of critical importance; too little insulin leads to diabetes, while an excess of insulin can cause potentially fatal hypoglycaemia. Yet, the pancreas of most people will control insulin secretion safely and effectively over decades and in response to glucose excursions driven by tens of thousands of meals. Because we only become aware of the important contributions of the pancreas when it fails to maintain glucose homeostasis, it is easy to forget just how well insulin release from a healthy pancreas is matched to insulin need to ensure stable blood glucose levels. Beta cells achieve this feat by extensive crosstalk with the rest of the endocrine cell types in the islet, notably the glucagon-producing alpha cells and somatostatin-producing delta cells. Here I will review the important paracrine contributions that each of these cells makes to the stimulation and subsequent inhibition of insulin release in response to a transient nutrient stimulation, and make the case that a breakdown of this local crosstalk contributes to the pathophysiology of diabetes.
Keywords Crosstalk . GABA . Glucagon . Pancreatic islet . Review . Serotonin . Somatostatin Abbreviations CRH Corticotropin-releasing hormone CRHR1 Type 1 corticotropin-releasing hormone receptor GABA γ-Aminobutyric acid GCGR Glucagon receptor GLP-1 Glucagon-like peptide 1 GLP-1R Glucagon-like peptide 1 receptor GPCR G protein-coupled receptor GSIS Glucose-stimulated insulin secretion 5-HT 5-Hydroxytryptamine PC Prohormone convertase UCN3 Urocortin-3
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00125-020-05213-5) contains a slideset of the figures for download, which is available to authorised users. * Mark O. Huising [email protected] 1
Department of Neurobiology, Physiology & Behavior, College of Biological Sciences, University of California, 196 Briggs Hall, 1 Shields Avenue, Davis, CA 95616, USA
2
Department of Physiology and Membrane Biology, School of Medicine, University of California, Davis, CA, USA
Introduction Because insulin deficiency is the common denominator across different forms of diabetes, the lion’s share of attention in the diabetes field for the pancreatic islets of Langerhans has, understandably, been focused on the beta cells. However, the islets are more than just the home of the insulinproducing beta cells. They contain several additional endocrine cell types, most notably glucagon-producing alpha cells and somatostatin-producing delta cells. These three endocrine cells share a common developmental origin and coordinate their activit
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