title: Ileal carbohydrates inhibit cholinergically stimulated exocrine pancreatic secretion in humans.
abstract: CONCLUSIONS
  Ileal inhibitory effects on pancreatic enzyme output are also demonstrable during exogenous, cholinergic stimulation of exocrine pancreatic secretion. These findings support the hypothesis that direct inhibition of cholinergic systems may be involved in the ileal inhibitory effects on pancreatic enzyme secretion. Furthermore, glucagon-like peptide-1 (GLP-1) may play a role in the mediation of the ileum-induced effects.
  
  
  BACKGROUND
  Ileal carbohydrate perfusion inhibits endogenously stimulated exocrine pancreatic secretion in humans. Our aim was to investigate if ileal perfusion of carbohydrates exerts similar effects on exogenously stimulated pancreatic enzyme output, i.e., if the inhibitory mechanisms are reproducible during direct, cholinergic stimulation of the exocrine pancreas. Furthermore, we sought to clarify the role of the potential humoral mediators (GLP-1) and peptide YY (PYY).
  
  
  METHODS
  Eight healthy fasting volunteers were intubated with an oroileal multilumen tube system for aspiration of duodenal juice and perfusion of test solutions. Exocrine pancreatic secretion was stimulated by a continuous i.v. infusion of the cholinergic agonist carbachol. Additionally, the ileum was perfused for 15-min intervals with either carbohydrates (total load: 18 g) or saline as control. Blood samples for determination of GLP-1 and PYY were taken before the beginning of exogenous stimulation and before and after ileal perfusion.
  
  
  RESULTS
  Exogenously stimulated pancreatic enzyme secretion was significantly inhibited by additional ileal carbohydrate perfusion (p < 0.05), whereas ileal saline had no effect. Moreover, plasma levels of GLP-1 increased significantly (p = 0.004) after ileal perfusion of carbohydrates, but not after saline. PYY plasma concentrations remained unchanged after both ileal perfusates.
authors.affiliation: Department of Medicine, University of Essen, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Gröger
authors.forename: A
authors.initials: A
authors.lastname: Unger
authors.forename: J J
authors.initials: JJ
authors.lastname: Holst
authors.forename: H
authors.initials: H
authors.lastname: Goebell
authors.forename: P
authors.initials: P
authors.lastname: Layer
mesh_terms: D000328:Adult; D000681:Amylases / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D050260:Carbohydrate Metabolism; D002241:Carbohydrates / Q000502:physiology*; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology*; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1; D006801:Humans; D007082:Ileum / Q000502:physiology*; D008049:Lipase / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D010446:Peptide Fragments / Q000097:blood; D019894:Peptide YY / Q000097:blood; D011498:Protein Precursors / Q000097:blood; D014357:Trypsin / Q000378:metabolism
chemical_list: D002241:Carbohydrates; D010446:Peptide Fragments; D011498:Protein Precursors; D019894:Peptide YY; D052216:Glucagon-Like Peptide 1; D002217:Carbachol; D005934:Glucagon; D008049:Lipase; D000681:Amylases; D014357:Trypsin