Alterations of AMPK, PI3K/Akt, and JNK independently associate with DM and ATM deficiency, and have been implicated in the inhibited glucose uptake and insulin resistance observed in both conditions. Further, aberrant metabolic conditions such as dyslipidemia, hyperinsulinemia, hyperglycemia and insulin resistance are features of DM and ATM deficiency, and contribute to vascular dysfunction. Mitochondrial dysfunction, increased ROS production and associated oxidative damage are also present in DM and during ATM deficiency. Lastly, DM and ATM deficiency independently associate with cardiac structural and functional abnormalities including increased cardiac fibrosis, hypertrophy, systolic and diastolic dysfunction. Collectively, all of the aforementioned conditions contributes to the development and progression of diabetic cardiomyopathy and heart failure.