G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation

G(i/o)-coupled somatostatin or α2-adrenergic receptor activation stimulated β-cell NKA activity, resulting in islet Ca(2+) fluctuations. Furthermore, intra-islet paracrine activation of β-cell G(i/o)-GPCRs and NKAs by δ-cell somatostatin secretion slowed Ca(2+) oscillations, which decreased insulin...

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Autores principales: Dickerson, Matthew T., Dadi, Prasanna K., Zaborska, Karolina E., Nakhe, Arya Y., Schaub, Charles M., Dobson, Jordyn R., Wright, Nicole M., Lynch, Joshua C., Scott, Claire F., Robinson, Logan D., Jacobson, David A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
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Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617941/
https://www.ncbi.nlm.nih.gov/pubmed/36309517
http://dx.doi.org/10.1038/s41467-022-34166-z
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author Dickerson, Matthew T.
Dadi, Prasanna K.
Zaborska, Karolina E.
Nakhe, Arya Y.
Schaub, Charles M.
Dobson, Jordyn R.
Wright, Nicole M.
Lynch, Joshua C.
Scott, Claire F.
Robinson, Logan D.
Jacobson, David A.
author_facet Dickerson, Matthew T.
Dadi, Prasanna K.
Zaborska, Karolina E.
Nakhe, Arya Y.
Schaub, Charles M.
Dobson, Jordyn R.
Wright, Nicole M.
Lynch, Joshua C.
Scott, Claire F.
Robinson, Logan D.
Jacobson, David A.
author_sort Dickerson, Matthew T.
collection PubMed
description G(i/o)-coupled somatostatin or α2-adrenergic receptor activation stimulated β-cell NKA activity, resulting in islet Ca(2+) fluctuations. Furthermore, intra-islet paracrine activation of β-cell G(i/o)-GPCRs and NKAs by δ-cell somatostatin secretion slowed Ca(2+) oscillations, which decreased insulin secretion. β-cell membrane potential hyperpolarization resulting from G(i/o)-GPCR activation was dependent on NKA phosphorylation by Src tyrosine kinases. Whereas, β-cell NKA function was inhibited by cAMP-dependent PKA activity. These data reveal that NKA-mediated β-cell membrane potential hyperpolarization is the primary and conserved mechanism for G(i/o)-GPCR control of electrical excitability, Ca(2+) handling, and insulin secretion.
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spelling pubmed-96179412022-10-31 G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation Dickerson, Matthew T. Dadi, Prasanna K. Zaborska, Karolina E. Nakhe, Arya Y. Schaub, Charles M. Dobson, Jordyn R. Wright, Nicole M. Lynch, Joshua C. Scott, Claire F. Robinson, Logan D. Jacobson, David A. Nat Commun Article G(i/o)-coupled somatostatin or α2-adrenergic receptor activation stimulated β-cell NKA activity, resulting in islet Ca(2+) fluctuations. Furthermore, intra-islet paracrine activation of β-cell G(i/o)-GPCRs and NKAs by δ-cell somatostatin secretion slowed Ca(2+) oscillations, which decreased insulin secretion. β-cell membrane potential hyperpolarization resulting from G(i/o)-GPCR activation was dependent on NKA phosphorylation by Src tyrosine kinases. Whereas, β-cell NKA function was inhibited by cAMP-dependent PKA activity. These data reveal that NKA-mediated β-cell membrane potential hyperpolarization is the primary and conserved mechanism for G(i/o)-GPCR control of electrical excitability, Ca(2+) handling, and insulin secretion. Nature Publishing Group UK 2022-10-29 /pmc/articles/PMC9617941/ /pubmed/36309517 http://dx.doi.org/10.1038/s41467-022-34166-z Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Dickerson, Matthew T.
Dadi, Prasanna K.
Zaborska, Karolina E.
Nakhe, Arya Y.
Schaub, Charles M.
Dobson, Jordyn R.
Wright, Nicole M.
Lynch, Joshua C.
Scott, Claire F.
Robinson, Logan D.
Jacobson, David A.
G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title_full G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title_fullStr G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title_full_unstemmed G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title_short G(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation
title_sort g(i/o) protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on na(+)/k(+) atpase activation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617941/
https://www.ncbi.nlm.nih.gov/pubmed/36309517
http://dx.doi.org/10.1038/s41467-022-34166-z
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