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- W2080580057 abstract "Gi-GPCRs, G protein-coupled receptors that signal via Gα proteins of the i/o class (Gαi/o), acutely regulate cellular behaviors widely in mammalian tissues, but their impact on the development and growth of these tissues is less clear. For example, Gi-GPCRs acutely regulate insulin release from pancreatic β cells, and variants in genes encoding several Gi-GPCRs--including the α-2a adrenergic receptor, ADRA2A--increase the risk of type 2 diabetes mellitus. However, type 2 diabetes also is associated with reduced total β-cell mass, and the role of Gi-GPCRs in establishing β-cell mass is unknown. Therefore, we asked whether Gi-GPCR signaling regulates β-cell mass. Here we show that Gi-GPCRs limit the proliferation of the insulin-producing pancreatic β cells and especially their expansion during the critical perinatal period. Increased Gi-GPCR activity in perinatal β cells decreased β-cell proliferation, reduced adult β-cell mass, and impaired glucose homeostasis. In contrast, Gi-GPCR inhibition enhanced perinatal β-cell proliferation, increased adult β-cell mass, and improved glucose homeostasis. Transcriptome analysis detected the expression of multiple Gi-GPCRs in developing and adult β cells, and gene-deletion experiments identified ADRA2A as a key Gi-GPCR regulator of β-cell replication. These studies link Gi-GPCR signaling to β-cell mass and diabetes risk and identify it as a potential target for therapies to protect and increase β-cell mass in patients with diabetes." @default.
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- W2080580057 date "2015-02-18" @default.
- W2080580057 modified "2023-10-14" @default.
- W2080580057 title "Gα <sub>i/o</sub> -coupled receptor signaling restricts pancreatic β-cell expansion" @default.
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- W2080580057 doi "https://doi.org/10.1073/pnas.1319378112" @default.
- W2080580057 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4352814" @default.
- W2080580057 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25695968" @default.
- W2080580057 hasPublicationYear "2015" @default.
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