GLPP could reverse the low expression of CYP7A1, FXR, SHP (small heterodimer partner) and other proteins and the high expression of FGFR4 in the liver of ob/ob mice and ApoC3 transgenic mice to regulate bile acid synthesis, and inhibit fatty acid synthesis by down-regulating the expression of SREBP1c, FAS, ACC, thereby ultimately improving NAFLD. Here, NR1H4 is linked to metabolic dysfunction-associated steatotic liver disease.