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Delta-cells and beta-cells are electrically coupled and regulate alpha-cell activity via somatostatin

Artikel i vetenskaplig tidskrift
Författare L. J. B. Briant
Thomas Reinbothe
I. Spiliotis
Caroline Miranda
B. Rodriguez
P. Rorsman
Publicerad i Journal of Physiology-London
Volym 596
Nummer/häfte 2
Sidor 197-215
ISSN 0022-3751
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 197-215
Språk en
Länkar doi.org/10.1113/JP274581
https://gup.ub.gu.se/file/207296
Ämnesord alpha cell, delta cell, beta cell, Islet cell, computer modelling, electrophysiology, somatostatin, inhibit glucagon-secretion, gap-junction channels, k-atp channels, pancreatic-islets, functional-characterization, insulin-release, glucose, control, mouse, paracrine, receptor, Neurosciences & Neurology
Ämneskategorier Neurologi, Fysiologi

Sammanfattning

Glucagon, the body's principal hyperglycaemic hormone, is released from alpha-cells of the pancreatic islet. Secretion of this hormone is dysregulated in type 2 diabetes mellitus but the mechanisms controlling secretion are not well understood. Regulation of glucagon secretion by factors secreted by neighbouring beta- and delta-cells (paracrine regulation) have been proposed to be important. In this study, we explored the importance of paracrine regulation by using an optogenetic strategy. Specific light-induced activation of beta-cells in mouse islets expressing the light-gated channelrhodopsin-2 resulted in stimulation of electrical activity in delta-cells but suppression of alpha-cell activity. Activation of the delta-cells was rapid and sensitive to the gap junction inhibitor carbenoxolone, whereas the effect on electrical activity in alpha-cells was blocked by CYN 154806, an antagonist of the somatostatin-2 receptor. These observations indicate that optogenetic activation of the beta-cells propagates to the delta-cells via gap junctions, and the consequential stimulation of somatostatin secretion inhibits alpha-cell electrical activity by a paracrine mechanism. To explore whether this pathway is important for regulating alpha-cell activity and glucagon secretion in human islets, we constructed computational models of human islets. These models had detailed architectures based on human islets and consisted of a collection of >500 alpha-, beta- and delta-cells. Simulations of these models revealed that this gap junctional/paracrine mechanism accounts for up to 23% of the suppression of glucagon secretion by high glucose.

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