In this study, we used HepG2 cells to establish a model of hepatocellular steatosis, and the effects of YCLLT on lipid deposition, inflammatory injury, mitochondrial dysfunction, and the AdipoR1/AMPK/SIRT1 signaling pathway of the model of hepatocellular steatosis, and to explore the possible molecular mechanisms by which YCLLT improves the hepatocellular steatosis, so that it will provide experimental bases for prevention and control of NAFLD as well as for the development of effective drugs. This evidence concerns the gene ADIPOR1 and metabolic dysfunction-associated steatotic liver disease.