These phytochemicals and their intestinal metabolites promoted the 5’-adenosine monophosphate-activated protein kinase (AMPK) pathway and/or protein kinase B (Akt) pathway, thereby stimulating the translocation of glucose transporter 4 (GLUT4) to the plasma membrane of L6 myoblasts or L6 myotubes under the condition of insulin absence, leading to the attenuation of hyperglycemia in T2D model db/db, ob/ob and KK-Ay/Ta mice, even under the condition of insulin resistance [12,13,14]. The gene discussed is AKT1; the disease is Insulin resistance.