title: Inhibitory effects of hyperglycaemia on fed jejunal motility: potential role of hyperinsulinaemia.
abstract: BACKGROUND
  Acute hyperglycaemia is known to inhibit jejunal interdigestive motility. This study was undertaken to establish the effects of hyperglycaemia on fed jejunal motility and small intestinal transit time, and to establish if the effects of hyperglycaemia are mediated in part by hyperinsulinaemia.
  
  
  METHODS
  Nine healthy male volunteers were studied in random order using three experimental conditions: (a) euglycaemic clamp [glucose 5 mmol L(-1)]; (b) hyperglycaemic clamp [glucose 15 mmol L(-1)]; and (c) euglycaemic hyperinsulinaemic clamp [glucose 5 mmol L(-l)]. Fed jejunal motility was induced by an intrajejunal perfusion of lipid (Lipofundin medium-chained triglyceride 10%) at 1.5 mL min(-1) [1.5 kcal min(-1)] for 180 min through the most proximal port of a manometry catheter (eight ports spaced at 2-cm intervals) located just distal to the ligament of Treitz. One minute after starting the lipid perfusion, 15 g of lactulose dissolved in 20 mL of tap water was infused. Small intestinal transit time was measured by the hydrogen breath test.
  
  
  RESULTS
  Acute hyperglycaemia reduced the total number of jejunal contractions and progradely propagated contractions, the motility index (P < 0.05) and the mean amplitude of contractions and delayed intestinal transit time. Hyperinsulinaemia reduced the total number of jejunal contractions, motility index (P < 0.05) and intestinal transit time.
  
  
  CONCLUSIONS
  Thus, hyperinsulinaemia may contribute to the inhibitory effects of hyperglycaemia on jejunal motility. In addition, this study demonstrated that intrajejunal infusion of lipid stimulates sustained glucagon-like peptide-1 release. In contrast to fat-induced gastric inhibitory polypeptide release, this glucagon-like peptide-1 release is not inhibited by exogenous or endogenous hyperinsulinaemia (P = 0.59).
authors.affiliation: Department of Gastroenterology and Endocrinology, University of Marburg, Germany. byrnem@mailer.uni-marburg.de
authors.forename: M M
authors.initials: MM
authors.lastname: Byrne
authors.forename: K
authors.initials: K
authors.lastname: Pluntke
authors.forename: U
authors.initials: U
authors.lastname: Wank
authors.forename: J
authors.initials: J
authors.lastname: Schirra
authors.forename: R
authors.initials: R
authors.lastname: Arnold
authors.forename: B
authors.initials: B
authors.lastname: Göke
authors.forename: M
authors.initials: M
authors.lastname: Katschinski
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D004338:Drug Combinations; D005769:Gastrointestinal Motility / Q000187:drug effects; D005772:Gastrointestinal Transit / Q000187:drug effects; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1; D015309:Glucose Clamp Technique; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology*; D006946:Hyperinsulinism / Q000097:blood / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007583:Jejunum / Q000503:physiopathology*; D008297:Male; D010191:Pancreatic Polypeptide / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010477:Perfusion; D010743:Phospholipids / Q000008:administration & dosage; D011498:Protein Precursors / Q000097:blood; D013012:Sorbitol / Q000008:administration & dosage
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D004338:Drug Combinations; D007328:Insulin; D010446:Peptide Fragments; D010743:Phospholipids; D011498:Protein Precursors; C008288:Lipofundin; D013012:Sorbitol; D010191:Pancreatic Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon