In HFD-induced cardiac hypertrophy and dysfunction, the absence of Sirt3 led to increased ROS generation and aggravated heart function compared with the WT mice, suggesting the significance of Sirt3 in preserving mitochondrial hemostasis and cardiac function during obesity-induced pathological hypertrophy (52). This evidence concerns the gene SIRT3 and obesity due to melanocortin 4 receptor deficiency.