Branched-chain amino acids prevent hepatic fibrosis and development of hepatocellular carcinoma in a non-alcoholic steatohepatitis mouse model

BCAA were administered to atherogenic and high-fat (Ath & HF) diet-induced nonalcoholic steatohepatitis (NASH) model mice and platelet-derived growth factor C transgenic mice (Pdgf-c Tg). Liver histology, tumor incidence, and gene expression profiles were evaluated. BCAA supplementation improved hepatic steatosis, inflammation, fibrosis, and tumors in the NASH mouse model, possibly through the modification of mTORC1 signaling. Using the Ath & HF diet mouse model, we investigated the effects of BCAA on steatosis, inflammation, fibrosis, and hepatocarcinogenesis in NASH.