Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK. Am J Physiol Gastrointest Liver Physiol 281: G924-G930, 2001.-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

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... ents of CLD. Acid output was significantly inhibited (50-60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6 Ϯ 0.3 to 4.8 Ϯ 0.5 pM) and lipid (4.6 Ϯ 0.5 pM). CCK levels 50-fold higher (218 Ϯ 33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol ⅐ kg Ϫ1 ⅐ h Ϫ1 iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9 Ϯ 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 Ϯ 1.9 pM) was significantly inhibited by CLD (14.5 Ϯ 3.6 pM), lipid (12.3 Ϯ 2.2 pM), and dextrose (11.9 Ϯ 1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.