Mechanisms of Gastric Emptying Disturbances in Chronic and Acute Inflammation of the Distal Gastrointestinal Tract
Research output: Contribution to journal › Journal article › Research › peer-review
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 vs. 182 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.
|Journal||American Journal of Physiology: Gastrointestinal and Liver Physiology|
|Publication status||Published - 2009|