Regulatory peptidesApr 7, 2009

Cholecystokinin and communication between the gut and brain

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 1, 2026

Abstract

Cholecystokinin (CCK) levels significantly influence the expression of appetite-related receptors in vagal afferent neurons.

Enteroendocrine cells in the gastrointestinal tract respond to food presence, regulating digestion and nutrient delivery.
Low plasma CCK levels during fasting lead to increased expression of cannabinoid CB1 and melanin concentrating hormone (MCH)-1 receptors, which may stimulate food intake.
Post-meal release of CCK down-regulates cannabinoid CB1 and MCH-1 receptors while up-regulating Y2 receptors in neurons connected to the stomach.
In fasting conditions, the expression of the appetite-stimulating neuropeptide MCH increases, while the satiety peptide cocaine and amphetamine regulated transcript (CART) decreases.
CCK secretion results in decreased MCH expression and increased CART expression, indicating a shift towards satiety signaling.
The neurochemical profile of vagal afferent neurons may reflect whether nutrients have been ingested recently, influencing appetite regulation.

Simplified

Enteroendocrine cells of the gastrointestinal tract act as a luminal surveillance system responding to either the presence or absence of food in the gut lumen. Collectively, their secretory products regulate the course of digestion and determine the delivery of nutrient to the gut by controlling food intake. Afferent neurons of the vagus nerve are an important target of gut hormones, particularly for control of food intake. The intestinal hormone cholecystokinin (CCK) stimulates vagal afferent neuron discharge and also controls the expression of both G-protein coupled receptors and peptide neurotransmitters in these neurons. When plasma CCK concentrations are low, for example in fasting, vagal afferent neurons express cannabinoid CB1 and melanin concentrating hormone (MCH)-1 receptors, both of which are associated with stimulation of food intake. Post-prandial release of CCK rapidly down-regulates the expression of both receptors but stimulates the expression of Y2 receptors in neurons projecting to the stomach. In fasting, there is also increased expression in these neurons of the appetite-stimulating neuropeptide transmitter MCH, and depressed expression of the satiety-peptide cocaine and amphetamine regulated transcript (CART). Secretion of CCK decreases expression of MCH and increases expression of CART. The neurochemical phenotype of vagal afferent neurons therefore encodes whether or not there has been nutrient ingestion over the previous period. At low plasma concentrations of CCK vagal afferent neurons exhibit increased capacity for appetite-stimulation, while post-prandial concentrations of CCK lead to enhanced capacity for satiety signalling. A gatekeeper function can therefore be attributed to CCK in that its presence or absence influences the capacity of vagal afferent neurons to respond to other neurohormonal signals.

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Cholecystokinin and communication between the gut and brain

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