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Hvidovre Hospital - en del af Københavns Universitetshospital
E-pub ahead of print

Glucagon Clearance is Preserved in Type 2 Diabetes

Publikation: Bidrag til tidsskriftTidsskriftartikelpeer review


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  2. C-peptide levels are ssociated with glycemic variability and hypoglycemia in insulin-treated type 2 diabetes

    Publikation: Bidrag til tidsskriftKonferenceabstrakt i tidsskriftpeer review

  • Magnus F G Grøndahl
  • Asger Lund
  • Jonatan I Bagger
  • Tonny S Petersen
  • Nicolai J Wewer Albrechtsen
  • Jens J Holst
  • Tina Vilsbøll
  • Mikkel B Christensen
  • Filip K Knop
Vis graf over relationer

Hyperglucagonemia is a common observation in both obesity and type 2 diabetes, and the etiology is primarily thought to be hypersecretion of glucagon. We investigated whether altered elimination kinetics of glucagon could contribute to the hyperglucagonemia in type 2 diabetes and obesity. Individuals with type 2 diabetes and preserved kidney function (8 with and 8 without obesity) and matched control individuals (8 with and 8 without obesity) were recruited. Each participant underwent a 1-hour glucagon infusion (4 ng/kg/min), achieving steady-state plasma glucagon concentrations, followed by a 1-hour wash-out period. Plasma levels, the metabolic clearance rate (MCR), half-life (T½) and volume of distribution of glucagon were evaluated and a pharmacokinetic model was constructed. Glucagon MCR and volume of distribution were significantly higher in the type 2 diabetes group compared to the control group, while no significant differences between the groups were found in glucagon T½ Individuals with obesity had neither a significantly decreased MCR, T½, nor volume of distribution of glucagon. In our pharmacokinetic model, glucagon MCR associated positively with fasting plasma glucose and negatively with body weight. In conclusion, our results suggest that impaired glucagon clearance is not a fundamental part of the hyperglucagonemia observed in obesity and type 2 diabetes.

StatusE-pub ahead of print - 26 okt. 2021

Bibliografisk note

© 2021 by the American Diabetes Association.

ID: 68600421