Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK

Kevin C K Lloyd, Jiafang Wang, Travis E. Solomon

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

We examined the role of CCK-A receptors in acid inhibition by intestinal nutrients. Gastric acid and plasma CCK and gastrin levels were measured in rats with gastric and duodenal fistulas during intragastric 8% peptone and duodenal perfusion with saline, complete liquid diet (CLD; 20% carbohydrate, 6% fat, and 5% protein), and the individual components of CLD. Acid output was significantly inhibited (50-60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6±0.3 to 4.8±0.5 pM) and lipid (4.6±0.5 pM). CCK levels 50-fold higher (218±33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol·kg-1·h-1 iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9±2.5 pM) without inhibiting acid secretion. The CCK-A antagonist MK-329 (1 mg/kg iv) reversed acid inhibition caused by CLD, lipid, and dextrose. Peptone-stimulated gastrin (21.7±1.9 pM) was significantly inhibited by CLD (14.5±3.6 pM), lipid (12.3±2.2 pM), and dextrose (11.9±1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume281
Issue number4 44-4
StatePublished - 2001

Keywords

  • Cholecystokinin
  • Enterogastrone
  • Gastric acid secretion
  • Intestinal phase
  • Peptone meal

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology
  • Physiology (medical)

Fingerprint Dive into the research topics of 'Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK'. Together they form a unique fingerprint.

  • Cite this