INS and Insulin resistance: In the insulin resistance HepG2 cell model induced by high glucose and high insulin, AME significantly increased the levels of rate-limiting enzymes for glucose oxidative decomposition, such as 6-phosphogluconate kinase, glucose kinase, and pyruvate kinase; reduced glucose synthesis by lowering glucose synthesis kinase-3-β (GSK-3-β) levels; and lowered phosphoenolpyruvate carboxy kinase and glucose-6-phosphate enzyme activity, thereby affecting the glucose biosynthesis pathway.