title: Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract.
abstract: 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 (13)C-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.
authors.affiliation: Israelitic Hospital, D-22297, Hamburg, Germany. keller@ik-h.de
authors.forename: Jutta
authors.initials: J
authors.lastname: Keller
authors.forename: Christoph
authors.initials: C
authors.lastname: Beglinger
authors.forename: Jens Juul
authors.initials: JJ
authors.lastname: Holst
authors.forename: Viola
authors.initials: V
authors.lastname: Andresen
authors.forename: Peter
authors.initials: P
authors.lastname: Layer
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002766:Cholecystokinin / Q000097:blood; D002908:Chronic Disease; D003093:Colitis, Ulcerative / Q000097:blood / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D003424:Crohn Disease / Q000097:blood / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D004239:Diverticulitis, Colonic / Q000097:blood / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D005215:Fasting / Q000097:blood; D005260:Female; D005746:Gastric Emptying / Q000502:physiology*; D005767:Gastrointestinal Diseases / Q000097:blood / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D019894:Peptide YY / Q000097:blood; D019518:Postprandial Period / Q000502:physiology; D013256:Steroids / Q000627:therapeutic use; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D013256:Steroids; D019894:Peptide YY; D052216:Glucagon-Like Peptide 1; D002097:C-Reactive Protein; D002766:Cholecystokinin