Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin- sensitive afferent pathway in rats

H. H. Holzer, C. M. Turkelson, T. E. Solomon, Helen E Raybould

Research output: Contribution to journalArticle

117 Citations (Scopus)

Abstract

The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid- induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume267
Issue number4 30-4
StatePublished - 1994
Externally publishedYes

Fingerprint

Afferent Pathways
Gastric Emptying
Capsaicin
Cholecystokinin
Lipids
Devazepide
Duodenum
Cholecystokinin A Receptor
Upper Gastrointestinal Tract
Stomach
Perfusion

Keywords

  • duodenum
  • gastric motility
  • sensory innervation

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin- sensitive afferent pathway in rats. / Holzer, H. H.; Turkelson, C. M.; Solomon, T. E.; Raybould, Helen E.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 267, No. 4 30-4, 1994.

Research output: Contribution to journalArticle

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