title: GLP-1 release in man after lower large bowel resection or intrarectal glucose administration.
abstract: BACKGROUND
  This study addresses the question whether the insulinotropic gut hormone, glucagon-like peptide-1 (GLP-1), is released from the lower large bowel upon oral or rectal glucose uptake.
  
  
  METHODS
  It was evaluated whether rectum or sigmoid colon resection alters glucose homeostasis or the plasma levels of the insulinotropic gut hormone, gastric inhibitory polypeptide (GIP), or GLP-1. Six men and 3 women (age 63 +/- 8 years, BMI 25.4 +/- 4.0 kg/m2) with normal preoperative fasting glucose values were treated before and after resection of large bowel segments. Fasting oral glucose tolerance (OGT, 75 g glucose/300 ml) tests were performed both before and 10 days postoperatively. Another approach aimed to clarify whether luminal glucose stimulation in the rectum/sigmoid colon increases GLP-1 plasma levels. Ten healthy volunteers (4 males, 6 females, age 25 +/- 2 years, BMI 22.1 +/- 2.4 kg/m2) received enemas with both saline and, 7 days later, 1 g/kg body weight glucose (70% glucose solution) intrarectally.
  
  
  RESULTS
  Neither rectum nor sigmoid colon resection led to significant changes in the pre- and postoperative glucose responses to OGT testing, or insulin, GIP and GLP-1 release. Intrarectal glucose instillation increased blood glucose by about 10 mg/dl with parallel small elevations in immunoreactive insulin and immunoreactive C peptide. However, plasma GLP-1 levels remained unaltered.
  
  
  CONCLUSIONS
  Our data make it unlikely that GLP-1 derived from the lower large bowel contributes significantly to maintain normal glucose tolerance.
authors.affiliation: Clinical Research Unit for Gastrointestinal Endocrinology, Department of Gastroenterology and Endocrinology, Philipps University of Marburg, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Printz
authors.forename: S
authors.initials: S
authors.lastname: Reiter
authors.forename: N
authors.initials: N
authors.lastname: Samadi
authors.forename: S
authors.initials: S
authors.lastname: Ebrahimsade
authors.forename: R
authors.initials: R
authors.lastname: Kirchner
authors.forename: R
authors.initials: R
authors.lastname: Arnold
authors.forename: B
authors.initials: B
authors.lastname: Göke
mesh_terms: D000285:Administration, Rectal; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000378:metabolism; D012809:Colon, Sigmoid / Q000601:surgery; D004733:Enema; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005934:Glucagon / Q000187:drug effects / Q000378:metabolism*; D052216:Glucagon-Like Peptide 1; D005947:Glucose / Q000008:administration & dosage*; D006801:Humans; D007328:Insulin / Q000097:blood; D007420:Intestine, Large / Q000187:drug effects / Q000378:metabolism* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000187:drug effects / Q000378:metabolism*; D011498:Protein Precursors / Q000187:drug effects / Q000378:metabolism*; D012002:Rectal Diseases / Q000601:surgery; D012007:Rectum / Q000601:surgery; D012810:Sigmoid Diseases / Q000601:surgery
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010446:Peptide Fragments; D011498:Protein Precursors; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D005947:Glucose