Therefore, in this study, we sought to determine whether these aforementioned changes in AgRP/NPY neuronal output were secondary to other HFD-induced changes (e.g., increased body weight and/or adiposity, hormone levels, etc) or if the persistent activation we observed in our previous study is an early consequence of HFD consumption that precedes and potentially contributes to other sequelae of overweight and obesity. This evidence concerns the gene NPY and obesity due to melanocortin 4 receptor deficiency.