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Apolipoprotein A-IV stimulates duodenal vagal afferent activity to inhibit gastric motility via a CCK₁ pathway

¹Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis 95616; ³Department of Biology, California State University Sacramento, Sacramento, California 95819; ²University Hospital, Department of General Surgery, University of Tübingen, 72074 Tübingen, Germany; ⁴Department of Surgery, Louisiana University School of Medicine, Shreveport, Louisiana 71130; and ⁵Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267

Submitted 9 December 2003 ; accepted in final form 13 April 2004

Apolipoprotein A-IV (apo A-IV), a peptide expressed by enterocytes in the mammalian small intestine and released in response to long-chain triglyceride absorption, may be involved in the regulation of gastric acid secretion and gastric motility. The specific aim of the present study was to determine the pathway involved in mediating inhibition of gastric motility produced by apo A-IV. Gastric motility was measured manometrically in response to injections of either recombinant purified apo A-IV (200 µg) or apo A-I, the structurally similar intestinal apolipoprotein not regulated by triglyceride absorption, close to the upper gastrointestinal tract in urethane-anesthetized rats. Injection of apo A-IV significantly inhibited gastric motility compared with apo A-I or vehicle injections. The response to exogenous apo A-IV injections was significantly reduced by 77 and 55%, respectively, in rats treated with the CCK₁ receptor blocker devazepide or after functional vagal deafferentation by perineural capsaicin treatment. In electrophysiological experiments, isolated proximal duodenal vagal afferent fibers were recorded in vitro in response to close-arterial injection of vehicle, apo A-IV (200 µg), or CCK (10 pmol). Apo A-IV stimulated the discharge of duodenal vagal afferent fibers, significantly increasing the discharge in 4/7 CCK-responsive units, and the response was abolished by CCK₁ receptor blockade with devazepide. These data suggest that apo A-IV released from the intestinal mucosa during lipid absorption stimulates the release of endogenous CCK that activates CCK₁ receptors on vagal afferent nerve terminals initiating feedback inhibition of gastric motility.

lipid; chylomicrons; mesenteric lymph; cholecytokinin

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