Altogether, these observations suggest that the obesity produced by hypothalamic nuclei lesions (VMH and PVN) and the dysregulation of brainstem melanocortin pathway(s) in the homeostatic control of food intake, body weight, and EE share similar metabolic and/ or neuro-anatomical substrates that may engage the vagus nerve, To test this hypothesis, we performed SDV in obese Mc4r−/− mice, and monitored their food intake and body weight. This evidence concerns the gene MC4R and obesity disorder.