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

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,...

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Bibliographic Details
Published in:American journal of physiology: Gastrointestinal and liver physiology 2001-10, Vol.281 (4), p.G924-G930
Main Authors: Lloyd, K C, Wang, J, Solomon, T E
Format: Article
Language:English
Subjects:
Animals
Cholecystokinin - blood
Devazepide - pharmacology
Diet
Duodenum - metabolism
Gastric Acid - metabolism
Gastric Acid - secretion
Gastric Mucosa - secretion
Gastrins - blood
Hormone Antagonists - pharmacology
Male
Nutritional Physiological Phenomena
Peptones - pharmacology
Perfusion
Rats
Rats, Sprague-Dawley
Receptor, Cholecystokinin A
Receptors, Cholecystokinin - metabolism
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Summary: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 x kg(-1) x 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.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.2001.281.4.g924