The vagus nerve is the primary neural mechanism for gut-brain communication. Vagal afferent neurons, located in the nodose ganglia, express numerous receptors that sense hormones released from the gut, and provide meal related information about the composition and quantity of food consumed to the brain. The gastrointestinal hormone, glucagon like peptide 1 (GLP1), released from enteroendocrine cells in response to a meal acts on GLP1 receptors located on vagal sensory nerve terminals in the gut to inhibit food intake, increase glucose clearance, and block gastric emptying. The mechanisms by which GLP1 produces these vagally-mediated physiological responses remains unknown. Recent evidence will be presented identifying a key role for the neuropeptide cocaine and amphetamine regulated transcript in vagal sensory neurons as a mediator of peripheral GLP1 signaling. Using an available single-cell RNA sequencing dataset obtained from mice nodose ganglia we characterized the extent of co-expression between Glp1r and several classic neuropeptides and identified the neuropeptide cocaine and amphetamine regulated transcript (CART) as having the highest level of co-expression with GLP1 receptor in nodose ganglia neurons. In situ hybridization demonstrates that CART and GLP1 receptor colocalization is conserved in rat nodose ganglia neurons. In rat primary cultures, GLP1 preferentially upregulates CART expression through a GLP1 receptor dependent mechanism. In vivo, viral mediated knockdown of CART in vagal sensory neurons blocks GLP1-induced satiation, gastric emptying, and alters circulating insulin levels. Similarly immunoneutralization of CART in the nucleus tractus solitarius, the site of vagal termination in the hindbrain, blunts GLP1-induced satiation and gastric emptying. Chemogenetic stimulation of CART expressing vagal sensory neurons in mice inhibits food intake, slows gastric emptying and alter glucose clearance in response to a meal. Together these data demonstrate that CART synthesis and release by vagal sensory neurons is necessary and sufficient to mediate the physiological response to peripheral GLP1.