Mechanisms of Gastric Emptying Disturbances in Chronic and Acute Inflammation of the Distal Gastrointestinal Tract

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Jutta Keller, Christoph Beglinger, Jens Juul Holst, Viola Andresen, Peter Layer

Objective: 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. Methods: 13 healthy subjects (CON), 13 patients with Crohn's disease (CD), 10 with ulcerative colitis (UC) and 7 with diverticulitis (DIV) underwent a standardized (13)C-octanoic acid gastric emptying breath test. Plasma glucose, cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) were measured periodically and correlated with GE parameters. Results (mean[SD]): Compared with CON, GE half time (T1/2) 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 T1/2 (>200min). Postprandial plasma glucose was increased in all patients, but was highest in DIV and correlated with T1/2 (R=0.90, p=0.006). In CD, mean postprandial CCK levels were increased threefold compared to CON (6.5[6.7] vs. 2.1[0.6] pmol/l, p=0.027) and were correlated with T1/2 (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). Conclusions: 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. Key words: inflammatory bowel disease, diverticulitis, motility, hormonal regulation.
Original languageEnglish
JournalAmerican Journal of Physiology: Gastrointestinal and Liver Physiology
ISSN0193-1857
DOIs
Publication statusPublished - 2009

ID: 18700424