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Am J Physiol Gastrointest Liver Physiol 281: G924-G930, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 4, G924-G930, October 2001

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

K. C. Kent Lloyd1, Jiafang Wang2,3, and Travis E. Solomon2,3

1 Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis 95616; 2 CURE: Digestive Diseases Research Center, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles 90073; and 3 Digestive Diseases Division, School of Medicine, University of California, Los Angeles, California 90024

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.

gastric acid secretion; enterogastrone; intestinal phase; cholecystokinin; peptone meal


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