Figure 9 shows that the compound may reverse AMPK/SIRT1/NF-κB activation, thereby reversing the increases in ADIPOQ, ADIPOR2, leptin, insulin, glucose levels, and resistin caused by HFD and decreasing NAFLD fatty acid β oxidation, oxidative stress, and inflammation, which inhibit lipid accumulation and improve the level of liver inflammation in NAFLD. This evidence concerns the gene LEP and metabolic dysfunction-associated steatotic liver disease.