| First Author | Dickerson MT | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 6461 |
| PubMed ID | 36309517 | Mgi Jnum | J:359393 |
| Mgi Id | MGI:7379573 | Doi | 10.1038/s41467-022-34166-z |
| Citation | Dickerson MT, et al. (2022) Gi/o protein-coupled receptor inhibition of beta-cell electrical excitability and insulin secretion depends on Na(+)/K(+) ATPase activation. Nat Commun 13(1):6461 |
| abstractText | Gi/o-coupled somatostatin or alpha2-adrenergic receptor activation stimulated beta-cell NKA activity, resulting in islet Ca(2+) fluctuations. Furthermore, intra-islet paracrine activation of beta-cell Gi/o-GPCRs and NKAs by delta-cell somatostatin secretion slowed Ca(2+) oscillations, which decreased insulin secretion. beta-cell membrane potential hyperpolarization resulting from Gi/o-GPCR activation was dependent on NKA phosphorylation by Src tyrosine kinases. Whereas, beta-cell NKA function was inhibited by cAMP-dependent PKA activity. These data reveal that NKA-mediated beta-cell membrane potential hyperpolarization is the primary and conserved mechanism for Gi/o-GPCR control of electrical excitability, Ca(2+) handling, and insulin secretion. |
