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Am J Physiol Gastrointest Liver Physiol 297: G861-G868, 2009. First published August 27, 2009; doi:10.1152/ajpgi.00145.2009
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NEUROREGULATION AND MOTILITY

Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract

Jutta Keller,1 Christoph Beglinger,2 Jens Juul Holst,3 Viola Andresen,1 and Peter Layer1

1Israelitic Hospital, Hamburg, Germany; 2Kantonsspital Basel, Switzerland; 3University of Copenhagen, Denmark

Submitted April 21, 2009 ; accepted in final form August 25, 2009

It is unclear why patients with inflammation of the distal bowel complain of symptoms referable to the upper gastrointestinal tract, specifically to gastric emptying (GE) disturbances. Thus we aimed to determine occurrence and putative pathomechanisms of gastric motor disorders in such patients. Thirteen healthy subjects (CON), 13 patients with Crohn's disease (CD), 10 with ulcerative colitis (UC), and 7 with diverticulitis (DIV) underwent a standardized 13C-octanoic acid gastric emptying breath test. Plasma glucose, CCK, peptide YY, and glucagon-like peptide-1 (GLP-1) were measured periodically and correlated with GE parameters. Results were given in means ± SD. Compared with CON, GE half time (T) was prolonged by 50% in CD (115 ± 55 vs. 182 ± 95 min, P = 0.037). Six CD, 2 DIV, and 2 UC patients had pathological T (>200 min). Postprandial plasma glucose was increased in all patients but was highest in DIV and correlated with T (r = 0.90, P = 0.006). In CD, mean postprandial CCK levels were increased threefold compared with CON (6.5 ± 6.7 vs. 2.1 ± 0.6 pmol/l, P = 0.027) and were correlated with T (r = 0.60, P = 0.041). Compared with CON, GLP-1 levels were increased in UC (25.1 ± 5.2 vs. 33.5 ± 13.0 pmol/l, P = 0.046) but markedly decreased in DIV (9.6 ± 5.2 pmol/l, P < 0.0001). We concluded that a subset of patients with CD, UC, or DIV has delayed GE. GE disturbances are most pronounced in CD and might partly be caused by excessive CCK release. In DIV there might be a pathophysiological link between decreased GLP-1 release, postprandial hyperglycemia, and delayed GE. These explorative data encourage further studies in larger patient groups.

inflammatory bowel disease; diverticulitis; motility; hormonal regulation



Address for reprint requests and other correspondence: J. Keller, Dept. of Internal Medicine, Israelitic Hospital, Univ. of Hamburg, Orchideenstieg 14, D-22297, Hamburg, Germany (e-mail: keller{at}ik-h.de).







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