Mediators for fat-induced ileal brake are different between stomach and proximal small intestine in conscious dogs.

Our aim was to determine the mechanisms by which intraileal fat alters proximal gastrointestinal motility--the ileal brake. Five mongrel dogs with ileal Thiry-Vella fistulas were equipped with strain gauge force transducers on the upper gut to measure contractile activity. Ileal infusions of 115 mmol/L oleic acid and triglyceride were studied in dogs with extrinsically innervated and extrinsically denervated Thiry-Vella loops. Plasma concentrations of peptide YY and total glucagon-like immunoactivity were measured. Oleic acid but not triglyceride inhibited postprandial contractions in the gastric antrum in dogs with innervated and denervated Thiry-Vella loops. Postprandial duodenal and jejunal motility was inhibited by oleic acid regardless of extrinsic denervation to the loops (P <0.05), but triglyceride inhibited small intestinal motility only in dogs with innervated Thiry-Vella loops. Intraileal oleic acid but not triglyceride increased plasma concentrations of peptide YY and total glucagon-like immunoactivity in dogs with innervated and denervated Thiry-Vella loops. Intraileal oleic acid inhibits gastric and small intestinal motility possibly via increased plasma concentrations of peptide YY and enteroglucagon. Intact extrinsic innervation is necessary for intraileal triglyceride to inhibit small intestinal motility.