Print Email Facebook Twitter Cholecystokinin regulates satiation independently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy Title Cholecystokinin regulates satiation independently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy Author Ripken, D. van der Wielen, N. van der Meulen, J. Schuurman, T. Witkamp, R.F. Hendriks, H.F.J. Koopmans, S.J. Publication year 2015 Abstract The vagal nerve and gut hormones CCK and GLP-1 play important roles in the control of food intake. However, it is not clear to what extent CCK and GLP-1 increase satiation by stimulating receptors located on abdominal vagal nerve endings or via receptors located elsewhere. This study aimed to further explore the relative contribution of the abdominal vagal nerve in mediating the satiating effects of endogenous CCK and GLP-1. Total subdiaphragmatic vagotomy or sham operation was combined with administration of CCK1 and GLP-1 receptor antagonists devazepide and exendin (9-39) in 12 pigs, applying an unbalanced Latin Square within-subject design. Furthermore, effects of vagotomy on preprandial and postprandial acetaminophen absorption, glucose, insulin, GLP-1 and CCK plasma concentrations were investigated.Ad libitum liquid meal intake (mean±SEM) was similar in sham and vagotomized pigs (4180±435 and 3760±810g/meal). Intake increased by about 20% after blockade of CCK1 receptors, independently of the abdominal vagal nerve. Food intake did not increase after blockade of GLP-1 receptors. Blockade of CCK1 and GLP-1 receptors increased circulating CCK and GLP-1 concentrations in sham pigs only, suggesting the existence of a vagal reflex mechanism in the regulation of plasma CCK1 and GLP-1 concentrations. Vagotomy decreased acetaminophen absorption and changed glucose, insulin, CCK and GLP-1 concentrations indicating a delay in gastric emptying. Our data show that at liquid feeding, satiation is decreased effectively by pharmacological blockade of CCK1 receptors. We conclude that regulation of liquid meal intake appears to be primarily regulated by CCK1 receptors not located on abdominal vagal nerve endings. Chemicals/CAS: cholecystokinin, 9011-97-6, 93443-27-7; devazepide, 103420-77-5; glucagon like peptide 1, 89750-14-1; glucose, 50-99-7, 84778-64-3; insulin, 9004-10-8; paracetamol, 103-90-2 Subject LifeMSB - Microbiology and Systems BiologyELSS - Earth, Life and Social SciencesBiomedical InnovationBiologyHealthy LivingCholecystokininDevazepideExendin (9-39)Food intake regulationGlucagon-like peptide 1Vagal nerveCholecystokininCholecystokinin A receptorGlucagon like peptide 1Glucagon like peptide 1 receptorGlucoseInsulinParacetamolAbdominal vagal nerveAnimal experimentAnimal modelAnimal tissueAutopsyCholecystokinin blood levelControlled studyDrug absorptionDrug blood levelFluid intakeFood intakeGlucose blood levelHormonal regulationHormone responseInsulin blood levelIntestine motilityMaleMaximum plasma concentrationNonhumanPostprandial statePatietySham procedureStomach absorptionStomach contentStomach emptyingSubdiaphragmatic vagotomyTime to maximum plasma concentrationVagotomyVagus nerveWeight gain To reference this document use: http://resolver.tudelft.nl/uuid:c1c50efd-16d2-42f7-86c1-a469c7cff16d DOI https://doi.org/10.1016/j.physbeh.2014.11.031 TNO identifier 520239 ISSN 0031-9384 Source Physiology and Behavior, 139, 167-176 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.