INTRACOLONIC FAT INHIBITS GASTRIC-ACID SECRETION INDEPENDENT OF GASTRIN-RELEASE IN THE DOG

The purpose of this study was to examine the effect of perfusion of the colon with a fatty acid (oleic acid) on peptone-stimulated gastric acid secretion and release of gastrin in conscious dogs. Gastric acid secretion was monitored by continuous intragastric titration. Perfusion of the colon with sodium oleate (24 mmol/hr) inhibited gastric acid secretion (14.2 +/- 2.6 meq/hr) stimulated by a peptone meal (1%) significantly (P < 0.05) when compared to perfusion of the colon with saline alone (20.1 +/- 1.6 meq/hr). The serum elevation in gastrin in response to intragastric instillation of the peptone meal was not affected by the colonic perfusion of oleic acid. Plasma concentrations of peptide YY (PYY) increased significantly in response to perfusion of the colon with saline or sodium oleate, and the integrated release of PYY in response to sodium oleate [6.9 +/- 2.8 ng (60-120) min/ml] was significantly greater than the response to saline [3.1 +/- 0.7 ng (60-120) min/ml]. The results of this study indicate that inhibition of gastric acid secretion by perfusion of the colon with fat is not due to an inhibition of gastrin release. In addition, because PYY is an inhibitor of gastric acid secretion, it is possible that PYY participates as an inhibitor of gastric acid secretion by the colon.