In conclusion, this study suggested that APL maybe a potential PPARγ agonist to improve insulin resistance via activating PPARγ and further regulating FGF21-AMPK signaling pathway, which therefore provide experimental evidences for developing APL as an attractive therapeutic drug for prevention and treatment of T2DM and other insulin resistance-related metabolic diseases such as nonalcoholic fatty liver disease. The gene discussed is FGF21; the disease is metabolic disease.