Cholecystokinin regulates satiation idependently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy

D. Ripken, N. van der Wielen, J. van der Meulen, T. Schuurman, R.F. Witkamp, H.F.J. Hendriks, S.J. Koopmans

Research output: Contribution to journalArticleAcademicpeer-review

10 Citations (Scopus)

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 ± 810 g/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.
LanguageEnglish
Pages167-176
JournalPhysiology and Behavior
Volume139
Issue number2015
DOIs
Publication statusPublished - 2015

Fingerprint

Satiation
Glucagon-Like Peptide 1
Vagotomy
Cholecystokinin
Swine
Meals
Nerve Endings
Acetaminophen
Eating
Devazepide
Insulin
Glucose
Gastric Emptying
Reflex
Hormones
Pharmacology

Keywords

  • glucagon-like peptide-1
  • food-intake
  • paracetamol absorption
  • physiological-role
  • appetite control
  • exendin 9-39
  • rats
  • glp-1
  • antagonist
  • afferents

Cite this

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title = "Cholecystokinin regulates satiation idependently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy",
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 ± 810 g/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.",
keywords = "glucagon-like peptide-1, food-intake, paracetamol absorption, physiological-role, appetite control, exendin 9-39, rats, glp-1, antagonist, afferents",
author = "D. Ripken and {van der Wielen}, N. and {van der Meulen}, J. and T. Schuurman and R.F. Witkamp and H.F.J. Hendriks and S.J. Koopmans",
year = "2015",
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language = "English",
volume = "139",
pages = "167--176",
journal = "Physiology and Behavior",
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Cholecystokinin regulates satiation idependently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy. / Ripken, D.; van der Wielen, N.; van der Meulen, J.; Schuurman, T.; Witkamp, R.F.; Hendriks, H.F.J.; Koopmans, S.J.

In: Physiology and Behavior, Vol. 139, No. 2015, 2015, p. 167-176.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Cholecystokinin regulates satiation idependently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy

AU - Ripken, D.

AU - van der Wielen, N.

AU - van der Meulen, J.

AU - Schuurman, T.

AU - Witkamp, R.F.

AU - Hendriks, H.F.J.

AU - Koopmans, S.J.

PY - 2015

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N2 - 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 ± 810 g/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.

AB - 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 ± 810 g/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.

KW - glucagon-like peptide-1

KW - food-intake

KW - paracetamol absorption

KW - physiological-role

KW - appetite control

KW - exendin 9-39

KW - rats

KW - glp-1

KW - antagonist

KW - afferents

U2 - 10.1016/j.physbeh.2014.11.031

DO - 10.1016/j.physbeh.2014.11.031

M3 - Article

VL - 139

SP - 167

EP - 176

JO - Physiology and Behavior

T2 - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

IS - 2015

ER -