Activation of vagal afferents in the rat duodenum by protein digests requires PepT1

N. P. Darcel, A. P. Liou, D. Tomé, Helen E Raybould

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


Intestinal infusion of protein digests activates a vago-vagal reflex inhibition of gastric motility. Protein digests release cholecystokinin (CCK) from enteroendocrine cells; however, the precise cellular mechanisms leading to vagal afferent activation is unclear. The hypothesis that the oligopeptide transporter PepT1 plays a major role in the initiation of this vago-vagal reflex was tested by recording activation of duodenal vagal afferent activity and inhibition of gastric motility in response to protein hydrolysates in the presence of 4-aminomethylbenzoic acid (4-AMBA), a competitive inhibitor of PepT1, or 4-aminophenylacetic acid (4-APAA), an inactive 4-AMBA analog. Duodenal infusion of the protein hydrolysate increased vagal afferent discharge and inhibited gastric motility; these responses were abolished by concomitant infusion of 4-AMBA, but not 4-APAA. Duodenal infusion with Cefaclor, a substrate of PepT1, increased duodenal vagal afferent activity; Cefaclor and protein hydrolysates selectively activated CCK-responsive vagal afferents. This study demonstrates that products of protein digestion increase spontaneous activity of CCK-sensitive duodenal vagal afferents via a mechanism involving the oligopeptide transporter PepT1.

Original languageEnglish (US)
Pages (from-to)1491-1495
Number of pages5
JournalJournal of Nutrition
Issue number6
StatePublished - Jun 2005


  • Cholecystokinin
  • Nutrient detection
  • PepT1
  • Protein
  • Vagal afferents

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science


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