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While the satiating effect of gut\u2010derived CCK on food\u2010intake control is well documented, the effect of peripheral GLP\u20101 is less clear. There is evidence that native GLP\u20101 can inhibit food intake only in the fed state but not in the fasting state. We therefore hypothesized that other gut peptides released during a meal might influence the subsequent effect of endogenous GLP\u20101 and investigated whether CCK could do so. We found that intraperitoneal injection of CCK in food\u2010restricted mice inhibited food intake during the first 30\u2010minute segment of a 1\u2010hour session of ad libitum chow intake and that mice compensated by increasing their intake during the second half of the session. Importantly, this compensatory behaviour was abolished by an intraperitoneal injection of GLP\u20101 administered following an intraperitoneal injection of CCK and prior to the 1\u2010hour session. In vivo activation of the free fatty acid 1 (FFA1) receptor with orally administered TAK875 increased plasma CCK concentration and, consistent with the effect of exogenous CCK, we found that prior oral administration of TAK875 increased the eating inhibitory effect of peripherally administered GLP\u20101. To examine the role of the vagus nerve in this effect, we utilized a saporin\u2010based lesioning procedure to selectively ablate the CCK receptor\u2010expressing gastrointestinal vagal afferent neurones (VANs). We found that the combined anorectic effect of TAK875 and GLP\u20101 was significantly attenuated in the absence of CCK receptor expressing VANs. Taken together, our results indicate that endogenous CCK interacts with GLP\u20101 to promote satiation and that activation of the FFA1 receptor can initiate this interaction by stimulating the release of CCK.<\/jats:p>","DOI":"10.1111\/dom.14575","type":"journal-article","created":{"date-parts":[[2021,10,19]],"date-time":"2021-10-19T20:49:25Z","timestamp":1634676565000},"page":"268-280","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Vagal afferent cholecystokinin receptor activation is required for glucagon\u2010like peptide\u20101\u2013induced satiation"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3249-4135","authenticated-orcid":false,"given":"Vasiliki","family":"Vana","sequence":"first","affiliation":[{"name":"Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences University of Copenhagen  Copenhagen Denmark"},{"name":"Novo Nordisk 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