title: Enhanced glucose-dependent glucagon-like peptide-1 and insulin secretion in Crohn patients with terminal ileum disease is unrelated to disease activity or ileal resection.
abstract: BACKGROUND
  Enhanced secretion of glucagon-like peptide-1 (GLP-1) has been reported in patients with Crohn disease (CD). However, the correlation between the enteropancreatic axis and the activity of CD remains unclear.
  
  
  METHODS
  Plasma glucose, insulin, GLP-1 levels and insulin sensitivity were determined before and after oral glucose tolerance tests in 13 patients with CD of the terminal ileum, in 13 patients after resection of the terminal ileum and in 7 healthy controls. Basal and stimulated insulin sensitivities were determined using the homeostasis model assessment (HOMA) and the insulin sensitivity index (ISI) methods, respectively.
  
  
  RESULTS
  Basal and stimulated glucose levels were comparable in patients and controls. The peak stimulated GLP-1 secretion was significantly higher in the patient group compared to controls: 12.2 +/- 1.24 pM/L and 8.1 +/- 1.72 pM/L, respectively, P=0.03. This was associated with 52% increased overall insulin secretion in the patients' group as compared to controls (P=0.007) and a higher peak insulin response: 63.5 +/- 9.69 mU/L and 41.5 +/- 6.85 mU/L for patients and controls, respectively, P=0.04. Operated patients had similar GLP-1 levels but higher peak and overall insulin secretions compared with those in non-operated patients (P=0.01). Fasting and stimulated insulin sensitivities were reduced only in patients with ileal resection as compared to controls: P=0.01 and P=0.05, respectively. No correlation was found between the CD activity index and GLP-1 or insulin secretion.
  
  
  CONCLUSIONS
  CD of the terminal ileum is associated with enhanced glucose-dependent GLP-1 secretion, which is unrelated to disease activity or ileal resection.
authors.affiliation: Division of Surgery, Institute of Gastroenterology, Assaf Harofeh Medical Center, Tel-Aviv University, Israel.
authors.forename: N
authors.initials: N
authors.lastname: Bendet
authors.forename: E
authors.initials: E
authors.lastname: Scapa
authors.forename: O
authors.initials: O
authors.lastname: Cohen
authors.forename: O
authors.initials: O
authors.lastname: Bloch
authors.forename: D
authors.initials: D
authors.lastname: Aharoni
authors.forename: Y
authors.initials: Y
authors.lastname: Ramot
authors.forename: M
authors.initials: M
authors.lastname: Weiss
authors.forename: A
authors.initials: A
authors.lastname: Halevi
authors.forename: M J
authors.initials: MJ
authors.lastname: Rapoport
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D016022:Case-Control Studies; D003424:Crohn Disease / Q000097:blood* / Q000503:physiopathology / Q000601:surgery; D005260:Female; D005934:Glucagon / Q000097:blood*; D052216:Glucagon-Like Peptide 1; D005951:Glucose Tolerance Test; D006706:Homeostasis; D006801:Humans; D007079:Ileitis / Q000097:blood* / Q000503:physiopathology / Q000601:surgery; D007082:Ileum / Q000601:surgery; D007328:Insulin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood*; D011498:Protein Precursors / Q000097:blood*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010446:Peptide Fragments; D011498:Protein Precursors; D052216:Glucagon-Like Peptide 1; D005934:Glucagon