The present study demonstrated that liver SREBP-1c, ChREBP, DGAT2, PPAR-α1 and MTP mRNA expression levels were all significantly decreased in iNOS-knockout mice fed an HFD for 48 weeks and that exhibited the progression of liver fibrosis, consistent with previous study results showing that the hepatic expression levels of genes involved in lipogenesis, fatty acid catabolism, and VLDL export in the liver were all suppressed during NASH pathogenesis [30]. Here, MLXIPL is linked to metabolic dysfunction-associated steatohepatitis.