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- W2621027948 abstract "While much is known about the molecular pathways that regulate embryonic development and adult homeostasis of the endocrine pancreas, little is known about what regulates early postnatal development and maturation of islets. Given that birth marks the first exposure to enteral nutrition, we investigated how nutrient-regulated signaling pathways influence postnatal islet development. To do this we performed loss-of-function studies of mechanistic target of rapamycin (mTOR), a highly conserved kinase within a nutrient-sensing pathway known to regulate cellular growth, morphogenesis and metabolism. Deletion of mTOR in pancreatic endocrine cells had no significant effect on their embryonic development. However, within the first 2 weeks after birth, mTOR-deficient islets became dysmorphic, β−cell maturation and function was impaired, and animals lost islet mass. Moreover, we discovered these distinct functions of mTOR are mediated by separate downstream branches of the pathway, in that mTORC1 (Raptor) is the main complex mediating maturation and function of islets, whereas mTORC2 (Rictor) impacts islet mass and architecture. Taken together, these findings suggest that nutrient-sensing may be a trigger for postnatal β cell maturation and islet development." @default.
- W2621027948 created "2017-06-09" @default.
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- W2621027948 date "2017-01-01" @default.
- W2621027948 modified "2023-10-08" @default.
- W2621027948 title "Distinct roles for the mTOR pathway in postnatal morphogenesis, maturation and function of pancreatic islets" @default.
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- W2621027948 doi "https://doi.org/10.1242/dev.146316" @default.
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