Irrespective of the carbohydrate quality of the diets, there was a down-regulation of GLUT4 expression in muscle and SAT, towards the end of the dietary intervention, which indicates an early progression toward insulin resistance and T2D pathogenesis as has been found in adipose tissue GLUT4 knockdown mice that developed insulin resistance [41], whereas overexpression of GLUT4 in adipocytes reduced fasting hyperglycemia and prevented insulin resistance [42]. Here, SLC2A4 is linked to Hyperglycemia.