Therefore, we selected the HFD-fed mouse model to investigate the efficacy of AMY for the prevention of NAFLD, and further aimed to establish the underlying molecular mechanism, analyzing AMP-activated protein kinase (AMPK), the mechanistic target of rapamycin complex 1 (mTORC1), and the sterol regulatory element binding protein 1 (SREBP1) transcriptions, which all have a pivotal role in hepatic lipid homeostasis (-, , 20). This evidence concerns the gene SREBF1 and metabolic dysfunction-associated steatotic liver disease.