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Am J Physiol Gastrointest Liver Physiol (February 5, 2004). doi:10.1152/ajpgi.00351.2003
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Submitted on August 14, 2003
Accepted on January 23, 2004

Cholecystokinin pathways modulate sensations induced by gastric distension in man

Simon Lal1*, John McLaughlin1, Josephine Barlow1, Massimo D'Amato2, Giampaolo Giacovelli2, Andrea Varro3, Graham J Dockray3, and David G Thompson1

1 Division of Gastro-Intestinal Sciences, Hope Hospital, University of Manchester, Manchester, United Kingdom
2 Rotta Research Laboratory, Monza, Italy
3 Department of Physiology, University of Liverpool, Liverpool, United Kingdom

* To whom correspondence should be addressed. E-mail: sll290{at}aol.com.

Ingested fat releases cholecystokinin (CCK), causes gastric relaxation, delays gastric emptying and limits meal size: however the mechanistic link between these actions has not been established. Fatty acid release of CCK is chain length sensitive: dodecanoic acid (C12) induces greater CCK release than decanoic acid (C10). The effect of C12 or C10 on tolerance to subsequent intragastric infusion of liquid was determined in healthy subjects, with and without the CCK1 receptor antagonist, dexloxiglumide. Gastric wall relaxation following either fatty acid was assessed by graded volume distension and by barostat; gastric emptying was measured by gastric aspiration and by a 13C octanoic acid breath technique. C12 released more CCK (mean plasma CCK after vehicle: 4.7±0.8pM; C10: 4.8±0.3pM; C12: 8±1.2pM; p<0.05 C12 vs. C10 or vehicle) and reduced the volume of water (and of 5% and 25% glucose solutions) delivered at maximum tolerance compared to C10 or vehicle (volume of water tolerated after veh: 1535±164 ml; C10: 1335±160ml; C12: 842±103ml; p<0.05 C12 vs. C10 or veh); this effect was abolished by dexloxiglumide. Intragastric volumes were always similar at the limit of tolerance, and, while gastric relaxation occurred to similar degrees following the fatty acids, its duration was longer after C12, which also induced a longer delay in gastric emptying (t1/2(min) after veh: 53±2; C10: 67±3; C12: 88±7 p<0.05 C12 vs. C10 or veh). In conclusion, ingestion of a CCK-releasing fatty acid reduces the tolerated volume of liquid delivered into the stomach, primarily via a CCK1 receptor-mediated delay in gastric emptying.




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