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- W59254232 abstract "Fluctuations in nutrients are sensed in cells and trigger a metabolic adaptive response to ensure homeostasis for energy and nutrients. For example, nutrient deprivation increases genes involved in mitochondrial fatty acid oxidation and glucose production. A key control occurs at the transcriptional level and coordinates the expression of metabolic genes. Among the major components of this transcriptional circuitry are the PGC-1α transcriptional coactivator complexes. Using skeletal muscle cells as a metabolic model system we found a nutrient sensing pathway that control fatty acid mitochondrial oxidative function. This pathway involves a response to low nutrients and glucose that in a cell-autonomous manner switches from glucose to fatty acid oxidation via an increase in a specific subset of mitochondrial genes. This coordination switch to fatty acid oxidation and full respiration activities is controlled through a mechanism of low glucose stimulated SIRT1-dependent deacetylation and activation of PGC-1α. De-acetylated PGC-1α is bound to promoters and activates genes involved in oxidation of fatty acids. In this regard, SIRT1 deficient cells lack the ability to undergo this nutrient switch under low glucose concentrations. Conversely, in high glucose concentrations PGC-1α is acetylated through the GCN5 Acetyl Transferase Complex, leading to decreases in mitochondrial fatty acid oxidation. Mechanistically, acetylation of PGC-1α results in inactivation of the transcriptional activity and displacement from the active chromatin to a different subnuclear localization. In summary, we have identified a nutrient-dependent molecular mechanisms that involve regulation of PGC-1α and mediate control of skeletal muscle mitochondrial nutrient oxidation activities." @default.
- W59254232 created "2016-06-24" @default.
- W59254232 creator A5070153869 @default.
- W59254232 date "2008-03-01" @default.
- W59254232 modified "2023-09-23" @default.
- W59254232 title "Nutrient Sensing Through Metabolic Transcription‐Dependent Acetylation" @default.
- W59254232 doi "https://doi.org/10.1096/fasebj.22.1_supplement.114.2" @default.
- W59254232 hasPublicationYear "2008" @default.
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