Experimental evidence demonstrates that Pue can reduce the expression of FATP 5, CD36, SREBF1, ChREBP, ACC, and FAS to decrease lipid uptake and biosynthesis, and up-regulate the expression of CPT 1a, ATGL, and ApoB100 to promote the degradation of lipids, which significantly improves the accumulation of lipids in the livers of rats with NAFLD (55). Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.