In rats, peripheral GLP-1-induced anorexia and neuronal activation of hypothalamic feeding circuits were both precluded by bilateral vagotomy or surgical transection of the brainstem-hypothalamic pathway.346 Likewise, selectively ablating nodose ganglionic neurons and the vagus nerve via systemic treatment with capsaicin completely blocks the anorectic effect of peripherally administered exendin-4 in mice.347 Collectively, these findings indicate that food reduction induced by peripheral GLP-1 is CNS-dependent. Here, GLP1R is linked to Anorexia.