title: Fasting and postprandial liver glycogen content in patients with type 1 diabetes mellitus after successful pancreas-kidney transplantation with systemic venous insulin delivery.
abstract: BACKGROUND
  In patients with type 1 diabetes mellitus (T1DM), insulin is usually replaced systemically (subcutaneously) and not via the physiological portal route. According to previous studies, the liver's capacity to store glycogen is reduced in T1DM patients, but it remains unclear whether this is due to hyperglycaemia, or whether the route of insulin supply could contribute to this phenomenon. T1DM patients after successful pancreas-kidney transplantation with systemic venous drainage (T1DM-PKT) represent a suitable human model to further investigate this question, because they are normoglycaemic, but their liver receives insulin from the pancreas transplant via the systemic route.
  
  
  METHODS
  In nine T1DM-PKT, nine controls without diabetes (CON) and seven patients with T1DM (T1DM), liver glycogen content was measured at fasting and after two standardized meals employing (13) C-nuclear-magnetic-resonance-spectroscopy. Circulating glucose and glucoregulatory hormones were measured repeatedly throughout the study day.
  
  
  RESULTS
  The mean and fasting concentrations of peripheral plasma glucose, insulin, glucagon and C-peptide were comparable between T1DM-PKT and CON, whereas T1DM were hyperglycaemic and hyperinsulinaemic (P < 0·05 vs T1DM-PKT and CON). Total liver glycogen content at fasting and after breakfast did not differ in the three groups. After lunch, T1DM-PKT and T1DM had a 14% and 21% lower total liver glycogen content than CON (P < 0·02).
  
  
  CONCLUSIONS
  In spite of normalized glycaemic control, postprandial liver glycogen content was reduced in T1DM-PKT with systemic venous drainage. Thus, not even optimized systemic insulin substitution is able to resolve the defect in postprandial liver glycogen storage seen in T1DM patients.
authors.affiliation: 3rd Medical Department of Metabolic Diseases and Nephrology, Hietzing Hospital, Vienna, Austria; Karl Landsteiner Institute of Metabolic Diseases and Nephrology, Vienna, Austria; Department of Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, UK.
authors.forename: M
authors.initials: M
authors.lastname: Stadler
authors.forename: M
authors.initials: M
authors.lastname: Krššák
authors.forename: D
authors.initials: D
authors.lastname: Jankovic
authors.forename: C
authors.initials: C
authors.lastname: Göbl
authors.forename: Y
authors.initials: Y
authors.lastname: Winhofer
authors.forename: G
authors.initials: G
authors.lastname: Pacini
authors.forename: M
authors.initials: M
authors.lastname: Bischof
authors.forename: M
authors.initials: M
authors.lastname: Haidinger
authors.forename: M
authors.initials: M
authors.lastname: Saemann
authors.forename: F
authors.initials: F
authors.lastname: Mühlbacher
authors.forename: M
authors.initials: M
authors.lastname: Korbonits
authors.forename: S M
authors.initials: SM
authors.lastname: Baumgartner-Parzer
authors.forename: A
authors.initials: A
authors.lastname: Luger
authors.forename: R
authors.initials: R
authors.lastname: Prager
authors.forename: C-H
authors.initials: CH
authors.lastname: Anderwald
authors.forename: M
authors.initials: M
authors.lastname: Krebs
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism / Q000601:surgery*; D005215:Fasting; D005260:Female; D005934:Glucagon / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood*; D016030:Kidney Transplantation; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D016035:Pancreas Transplantation; D019518:Postprandial Period; D011863:Radioimmunoassay
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D008112:Liver Glycogen; D005934:Glucagon