The vagus nerve have been recognized as the core of the gut-brain axis that provides a neural pathway connecting the gut and central nervous system (CNS). Vagal sensory neurons residing in the nodose ganglia (NG), convey information of meal-borne signals to the brain, providing an important negative-feedback mechanism for meal size regulation. The neuropeptide cocaine and amphetamine regulated-transcript (CART) is a good candidate because CART is released from the vagus nerve into the NTS in response to a meal and is sufficient and necessary for meal termination. Moreover, CART expression and signaling are disrupted in obesity, and genetic manipulation of the vagus nerve to replicate these disruptions promote overeating and weight gain. Interestingly, vagus nerve stimulation has been shown to be effective for weight loss. Therefore we hypothesize that activation of CART expressing NG neurons will cause a reduction in food intake and body in obese mice.