Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Regul Pept. 2009 Jun 5;155(1-3):6-10. doi: 10.1016/j.regpep.2009.03.015. Epub 2009 Apr 2.

Cholecystokinin and gut-brain signalling.

Author information

  • Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Crown St, Liverpool L69 3BX, UK. g.j.dockray@liverpool.ac.uk

Abstract

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.

PMID:
19345244
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk