In the model of non-alcoholic fatty liver disease, LBPs treatment significantly reduced the intracellular lipid accumulation and concentrations of TG, alanine aminotransferase (ALT), aspartate transaminase (AST), and malondialdehyde, while increasing the concentrations of SOD, phospholipid hydroperoxides, GSH-Px, and CAT [108]. Here, GPT is linked to metabolic dysfunction-associated steatotic liver disease.