Inhibition of gastric emptying in response to intestinal lipid is dependent on chylomicron formation.

Published

Journal Article

Lipid in the intestine initiates feedback inhibition of proximal gastrointestinal function and food intake. In rats and humans, inhibition of gastric emptying is mediated, at least in part, by cholecystokinin (CCK)-A receptors, and in rats there is evidence for involvement of an intestinal vagal afferent pathway. The mechanism by which luminal lipid acts to release CCK or activate vagal afferent nerve terminals is unclear. The role of chylomicron formation in this sensory transduction pathway has been investigated using the hydrophobic surfactant Pluronic L-81 that inhibits chylomicron formation. Gastric emptying of liquids was measured in awake rats fitted with a Thomas gastric fistula and a duodenal cannula. Intestinal perfusion of lipid induced a dose-dependent inhibition of gastric emptying (6, 12, and 39% inhibition for 25, 50, and 100 mg lipid, respectively). Perfusion of lipid with Pluronic L-81 (2.8% wt/vol) reversed the lipid-induced inhibition of gastric emptying. Pluronic L-63, a chemically similar surfactant that has no effect on chylomicron formation, had no effect on lipid-induced inhibition of gastric emptying. Perfusion of the intestine with lipid (100 mg) increased plasma levels of CCK from 1.9 ± 0.8 to 6.5 ± 1 pM. This increase was blocked by Pluronic L-81 but unaffected by L-63. These results provide evidence that chylomicron formation is important in the signaling of lipid in the intestinal lumen to CCK endocrine cells and to producing feedback inhibition of gastric emptying.

Full Text

Duke Authors

Cited Authors

  • Raybould, HE; Meyer, JH; Tabrizi, Y; Liddle, RA; Tso, P

Published Date

  • June 1, 1998

Published In

Volume / Issue

  • 274 / 6

Start / End Page

  • R1834 - R1838

PubMed ID

  • 29586675

Pubmed Central ID

  • 29586675

Electronic International Standard Serial Number (EISSN)

  • 1522-1490

Digital Object Identifier (DOI)

  • 10.1152/ajpregu.1998.274.6.R1834

Language

  • eng

Conference Location

  • United States