In senescence-accelerated mice prone 8 (SAMP8), EGCG supplementation (3.2 g EGCG/kg chow diet) for 12 weeks improves insulin resistance by enhancing AMPKα activity, restoring Akt activity, recovering GLUT4 protein expression, and augmenting mitochondrial biogenesis in the skeletal muscle, and alleviates hepatic fat deposition by downregulating mTOR and SREBP-1c-mediated lipid biosynthesis via suppressing the positive regulator Akt and activating the negative regulator AMPKα in the liver [131]. This evidence concerns the gene AKT1 and Insulin resistance.