title: Type I diabetes mellitus does not alter initial splanchnic glucose extraction or hepatic UDP-glucose flux during enteral glucose administration.
abstract: OBJECTIVE
  Our aim was to determine whether an alteration in splanchnic glucose metabolism could contribute to postprandial hyperglycaemia in people with Type I (insulin-dependent) diabetes mellitus.
  
  
  METHODS
  Splanchnic glucose extraction, hepatic glycogen synthesis and endogenous glucose production were compared in 8 Type I diabetic patients and in 11 control subjects. Endogenous hormone secretion was inhibited with somatostatin while insulin (approximately 550 pmol/l) and glucagon (approximately 130 ng/l) concentrations were matched with exogenous hormone infusions. Glucose containing [3-3H] glucose was infused into the duodenum at a rate of 20 micromol.kg(-1).min(-1). Plasma glucose concentrations were maintained at about 8.5 mmol/l in both groups by means of a separate variable intravenous glucose infusion.
  
  
  RESULTS
  Initial splanchnic glucose uptake, calculated by subtracting the systemic rate of appearance of [3-3H] glucose from the rate of infusion of [3-3H] glucose into the duodenum, did not differ in the diabetic and non-diabetic patients (4.1 +/- 0.8 vs 3.0 +/- 1.0 micromol/kg/min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide method did not differ (10.7 +/- 2.4 vs 10.1 +/- 2.7 micromol.kg(-1).min(-1)). On the other hand, suppression of endogenous glucose production, measured by an intravenous infusion of [6,6-2H2] glucose, was greater (p < 0.05) in the diabetic than in the non-diabetic subjects (1.7 +/- 1.6 vs 5.8 +/- 1.9 micromol.kg(-1).min(-1)).
  
  
  CONCLUSIONS
  When glucose, insulin and glucagon concentrations are matched in individuals with relatively good chronic glycaemic control, Type I diabetes does not alter initial splanchnic glucose uptake of enterally delivered glucose or hepatic glycogen synthesis. Alterations in splanchnic glucose metabolism are not likely to contribute to postprandial hyperglycaemia in people with well controlled Type I diabetes.
authors: Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
authors: A
authors: A
authors: Vella
authors: P
authors: P
authors: Shah
authors: R
authors: R
authors: Basu
authors: A
authors: A
authors: Basu
authors: M
authors: M
authors: Camilleri
authors: W F
authors: WF
authors: Schwenk
authors: R A
authors: RA
authors: Rizza
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D002096:C-Peptide / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D004386:Duodenum; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology*; D006728:Hormones / Q000097:blood; D006801:Humans; D007267:Injections; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism*; D012016:Reference Values; D014530:Uridine Diphosphate / Q000378:metabolism*; D014781:Viscera / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D006728:Hormones; D007328:Insulin; D014530:Uridine Diphosphate; D005947:Glucose