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Am J Physiol Gastrointest Liver Physiol 276: G550-G555, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 2, G550-G555, February 1999

Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY

Xiao-Tuan Zhao, John H. Walsh, Helen Wong, Lijie Wang, and Henry C. Lin

Department of Medicine, Cedars-Sinai Burns and Allen Research Institute, Cedars-Sinai Medical Center, Los Angeles 90048; and CURE: Digestive Disease Research Center and University of California, Los Angeles, California 90024

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat (P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist (P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist (P < 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

gastrointestinal motility; stomach; small intestine; gut peptide


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