PPARGC1A and Insulin resistance: These results are consistent with the possibility that a deficiency of GLUT-4 and p-AMPK-α2 expression contributes to decreased glucose transport and increased insulin resistance in diabetic obese rats, because activation of GLUT-4 and AMPK in skeletal muscle may enhance insulin-stimulated glucose transport and glycogen content and lead to increases in fat oxidation, induction of PGC-1α and genes governing mitochondrial biogenesis and enzymes of oxidation phosphorylation6, 13, 16, 18.