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1 Anatomy, Physiology and Cell Biology, University of California, Davis School of Veterinary Medicine, Davis, CA, USA; General Surgery, University of Tubingen, Tubingen, Germany
2 Anatomy, Physiology and Cell Biology, University of California, Davis School of Veterinary Medicine, Davis, CA, USA
3 Anatomy, Physiology and Cell Biology, University of California, Davis School of Veterinary Medicine, Davis, CA, USA; Biology, CSUS, Sacramento, CA, USA
4 Surgery, LSU School of Medicine, Shreveport, LA, USA
5 Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: heraybould{at}ucdavis.edu.
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 to 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 following functional vagal differentiation by per neural 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) orCCK (10 pool). Apo A-IV stimulated the discharge of duodenal vagal afferent fibers, significantly increasing the discharge in 4/7 CCK-responsive units, 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.
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