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Decanoic acid inhibits mTORC1 activity independent of glucose and insulin signaling

Nevertheless, the variability in clinical outcomes indicates a pressing need for more focused, mechanism-based research

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Moreover, also a by-product of ethanol metabolism such as acetaldehyde, which is further oxidised to acetate by mitochondrial aldehyde dehydrogenase, seems to contribute primarily to the alcohol-induced liver diseases by acting at the genomic level through up-regulation of some redox-sensitive transcription factors involved in fibrogen-esis, such as AP-1 and NF-B

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