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

Matthew T. Dickerson, Prasanna K. Dadi, Karolina E. Zaborska, Arya Y. Nakhe, Charles M. Schaub, Jordyn R. Dobson, Nicole M. Wright, Joshua C. Lynch, Claire F. Scott, Logan D. Robinson and David A. Jacobson ()
Additional contact information
Matthew T. Dickerson: Vanderbilt University
Prasanna K. Dadi: Vanderbilt University
Karolina E. Zaborska: Vanderbilt University
Arya Y. Nakhe: Vanderbilt University
Charles M. Schaub: Vanderbilt University
Jordyn R. Dobson: Vanderbilt University
Nicole M. Wright: Vanderbilt University
Joshua C. Lynch: Vanderbilt University
Claire F. Scott: Vanderbilt University
Logan D. Robinson: Vanderbilt University
David A. Jacobson: Vanderbilt University

Nature Communications, 2022, vol. 13, issue 1, 1-18

Abstract: Abstract Gi/o-coupled somatostatin or α2-adrenergic receptor activation stimulated β-cell NKA activity, resulting in islet Ca2+ fluctuations. Furthermore, intra-islet paracrine activation of β-cell Gi/o-GPCRs and NKAs by δ-cell somatostatin secretion slowed Ca2+ oscillations, which decreased insulin secretion. β-cell membrane potential hyperpolarization resulting from Gi/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 Gi/o-GPCR control of electrical excitability, Ca2+ handling, and insulin secretion.

Date: 2022
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DOI: 10.1038/s41467-022-34166-z

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