We reported for the first time that the effects of AM on acquired hyperlipidemia are likely achieved by regulating the lipid metabolism, it markedly reduced the process of lipogenesis, and increased the process of lipolysis and lipid β-oxidation in liver tissue and WAT; moreover, the key targets of AM might be AKT1, VEGFA, CCND1 and ESR1. This evidence concerns the gene AKT1 and hyperlipidemia.