In summary, we found that in insulin-stimulated cardiomyocytes of MetS rats, an impaired glucose uptake and Akt activation occurs, and also Akt decreases its interaction with proteins related to energy metabolism and some positive regulators, and increases its interaction with proteins related to contraction, ER stress, and IR, a redistribution manner that reflects the impaired glucose metabolism and Akt signaling in the heart. This evidence concerns the gene AKT1 and metabolic syndrome.