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• W2060759722 startingPage "16876" @default.
• W2060759722 abstract "Under feeding conditions, the incretin hormone GLP-1 promotes pancreatic islet viability by triggering the cAMP pathway in beta cells. Increases in PKA activity stimulate the phosphorylation of CREB, which in turn enhances beta cell survival by upregulating IRS2 expression. Although sustained GLP-1 action appears important for its salutary effects on islet function, the transient nature of CREB activation has pointed to the involvement of additional nuclear factors in this process. Following the acute induction of CREB-regulated genes, cAMP triggers a second delayed phase of gene expression that proceeds via the HIF transcription factor. Increases in cAMP promote the accumulation of HIF1α in beta cells by activating the mTOR pathway. As exposure to rapamycin disrupts GLP-1 effects on beta cell viability, these results demonstrate how a pathway associated with tumor growth also mediates salutary effects of an incretin hormone on pancreatic islet function." @default.
• W2060759722 created "2016-06-24" @default.
• W2060759722 creator A5030928703 @default.
• W2060759722 creator A5046795714 @default.
• W2060759722 creator A5072518932 @default.
• W2060759722 date "2011-09-26" @default.
• W2060759722 modified "2023-10-04" @default.
• W2060759722 title "mTOR links incretin signaling to HIF induction in pancreatic beta cells" @default.
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• W2060759722 doi "https://doi.org/10.1073/pnas.1114228108" @default.
• W2060759722 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3193251" @default.
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