title: Effects of physiological hyperglycemia on duodenal motility and flow events, glucose absorption, and incretin secretion in healthy humans.
abstract: BACKGROUND
  Acute hyperglycemia slows gastric emptying, but its effects on small intestinal motor activity and glucose absorption are unknown. In type 2 diabetes, the postprandial secretion of glucose-dependent insulinotropic polypeptide (GIP) is preserved, but that of glucagon-like peptide-1 (GLP-1) is possibly reduced; whether the latter is secondary to hyperglycemia or diabetes per se is unknown.
  
  
  OBJECTIVE
  The aim was to investigate the effects of acute hyperglycemia on duodenal motility and flow events, glucose absorption, and incretin hormone secretion.
  
  
  METHODS
  Nine healthy volunteers were studied on two occasions. A combined manometry/impedance catheter was positioned in the duodenum. Blood glucose was clamped at either 9 mmol/liter (hyperglycemia) or 5 mmol/liter (euglycemia) throughout the study. Manometry and impedance recordings continued between T=-10 min and T=180 min. Between T=0 and 60 min, an intraduodenal glucose infusion was given (approximately 3 kcal/min), together with 14C-labeled 3-O-methylglucose (3-OMG) to evaluate glucose absorption.
  
  
  RESULTS
  Hyperglycemia had no effect on duodenal pressure waves or flow events during the 60 min of intraduodenal glucose infusion, when compared to euglycemia. During hyperglycemia, there was an increase in plasma GIP (P<0.05) and 14C-3-OMG (P<0.05) but no effect on GLP-1 concentrations in response to the intraduodenal infusion, compared to euglycemia.
  
  
  CONCLUSIONS
  Acute hyperglycemia in the physiological range has no effect on duodenal pressure waves and flow events but is associated with increased GIP secretion and rate of glucose absorption in response to intraduodenal glucose.
authors.affiliation: Discipline of Medicine, University of Adelaide, Level 6, Eleanor Harrald Building, Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Paul
authors.initials: P
authors.lastname: Kuo
authors.forename: Judith M
authors.initials: JM
authors.lastname: Wishart
authors.forename: Max
authors.initials: M
authors.lastname: Bellon
authors.forename: André J
authors.initials: AJ
authors.lastname: Smout
authors.forename: Richard H
authors.initials: RH
authors.lastname: Holloway
authors.forename: Robert J L
authors.initials: RJ
authors.lastname: Fraser
authors.forename: Michael
authors.initials: M
authors.lastname: Horowitz
authors.forename: Karen L
authors.initials: KL
authors.lastname: Jones
authors.forename: Christopher K
authors.initials: CK
authors.lastname: Rayner
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D019540:Area Under Curve; D001786:Blood Glucose / Q000378:metabolism*; D004386:Duodenum / Q000187:drug effects* / Q000502:physiology; D017097:Electric Impedance; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005769:Gastrointestinal Motility / Q000187:drug effects*; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D054795:Incretins / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008297:Male; D008365:Manometry; D016037:Single-Blind Method
chemical_list: D001786:Blood Glucose; D054795:Incretins; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D005947:Glucose