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Modulation of hepatocellular redox, lipid oxidation and de novo lipogenesis by BCAAs. Chronic supplementation of BCAAs maintains hepatic insulin sensitivity while altering mitochondrial NADH:NAD+ ratio, activating fed-to-fasted phosphorylation of AMPKα and ACC. The higher NADH:NAD+ ratio and the activation of AMPKα primes the liver to oxidize free fatty acids, whereas the inhibitory phosphorylation of ACC helps downregulate DNL in the liver. BCAA, branched-chain amino acid.
