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Nutritional Neurosciences

Activation of Vagal Afferents in the Rat Duodenum by Protein Digests Requires PepT1^1,2

Department of Anatomy, Physiology and Cell Biology, UC Davis School of Veterinary Medicine, Davis, CA 95616 and ^* UMR INRA 914 Physiologie de la Nutrition et du Comportement Alimentaire, INAPG, 75231 Paris cedex 05, France

³To whom correspondence should be addressed. E-mail: heraybould{at}ucdavis.edu.

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.

KEY WORDS: • nutrient detection • protein • vagal afferents • PepT1 • cholecystokinin

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