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- W2034359103 abstract "Fatty acids can favour the development of Type 2 diabetes by reducing insulin secretion and inducing apoptosis of pancreatic β-cells. Here, we show that sustained exposure of the β-cell line MIN6 or of isolated pancreatic islets to the most abundant circulating fatty acid palmitate increases the level of C/EBPβ, an insulin transcriptional repressor. In contrast, two unsaturated fatty acids, oleate and linoleate were without effect. The induction of C/EBPβ elicited by palmitate was prevented by inhibiting the ERK1/2 MAP kinase pathway or by reducing mitochondrial fatty acid oxidation with an inhibitor of Carnitine Palmitoyl Transferase-1. Overexpression of C/EBPβ mimicked the detrimental effects of palmitate and resulted in a drastic reduction in insulin promoter activity, impairment in the capacity to respond to secretory stimuli and an increase in apoptosis. Our data suggest a potential involvement of C/EBPβ as mediator of the deleterious effects of unsaturated free fatty acids on β-cell function." @default.
- W2034359103 created "2016-06-24" @default.
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- W2034359103 date "2009-06-01" @default.
- W2034359103 modified "2023-09-27" @default.
- W2034359103 title "Role of the transcriptional factor C/EBPβ in free fatty acid-elicited β-cell failure" @default.
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- W2034359103 doi "https://doi.org/10.1016/j.mce.2008.12.005" @default.
- W2034359103 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19133313" @default.
- W2034359103 hasPublicationYear "2009" @default.
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