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

Dec 3, 2014Physiology & behavior

Cholecystokinin controls fullness without the abdominal vagal nerve in pigs with full nerve cut below the diaphragm

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Abstract

Ad libitum liquid meal intake was similar in sham and vagotomized pigs at 4180±435 g and 3760±810 g per meal, respectively.

Blockade of CCK1 receptors increased food intake by about 20%, suggesting their significant role in controlling satiation.
Food intake did not increase after blocking GLP-1 receptors, indicating that GLP-1 may not directly influence meal satiation in this context.
Blockade of CCK1 and GLP-1 receptors resulted in increased levels of CCK and GLP-1 only in sham-operated pigs, implying a vagal reflex mechanism in their regulation.
Vagotomy led to decreased acetaminophen absorption and altered plasma concentrations of glucose, insulin, CCK, and GLP-1, indicating delayed gastric emptying.

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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.

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

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