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- W3027979596 abstract "Abstract Compromised β-cell identity is emerging as an important contributor to β-cell failure in diabetes; however, the precise mechanism independent of hyperglycemia is under investigation. We have previously reported that mTORC1/ Rapto r regulates functional maturation in β-cells. In the present study, we find that diabetic β-cell specific Raptor -deficient mice (βRapKO GFP ) show reduced β-cell mass, loss of β-cell identity and acquisition of α-cell features; which are not reversible upon glucose normalization. Deletion of Raptor directly impairs β-cell identity, mitochondrial metabolic coupling and protein synthetic activity, leading to β-cell failure. Moreover, loss of Raptor activates α-cell transcription factor MafB (via modulating C/EBPβ isoform ratio) and several α-cell enriched genes i.e. Etv1 and Tspan12 , thus initiates β- to α-cell reprograming. The present findings highlight mTORC1 as a metabolic rheostat for stabilizing β-cell identity and repressing α-cell program at normoglycemic level, which might present therapeutic opportunities for treatment of diabetes." @default.
- W3027979596 created "2020-05-29" @default.
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- W3027979596 date "2020-05-21" @default.
- W3027979596 modified "2023-10-17" @default.
- W3027979596 title "Raptor determines β-cell identity and plasticity independent of hyperglycemia in mice" @default.
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- W3027979596 doi "https://doi.org/10.1038/s41467-020-15935-0" @default.
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- W3027979596 hasPublicationYear "2020" @default.
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