Plasma levels of glucagon but not GLP-1 are elevated in response to inflammation in humans

in Endocrine Connections
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  • 1 J Modrzynska, Department of Biomedical Sciences, University of Copenhagen Faculty of Health and Medical Sciences, Kobenhavn, Denmark
  • 2 C Klein, Department of Cardiology, Herlev Gentofte Hospital, Herlev, Denmark
  • 3 K Iversen, Department of Clinical Medicine, Herlev Gentofte Hospital, Herlev, Denmark
  • 4 H Bundgaard, Department of Cardiology, Rigshospitalet, Kobenhavn, Denmark
  • 5 B Hartmann, Department of Biomedical Sciences, University of Copenhagen Faculty of Health and Medical Sciences, Kobenhavn, Denmark
  • 6 M Moss, Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
  • 7 N Rittig, Steno Diabetes Center, Aarhus University Hospital, Aarhus, Denmark
  • 8 N Moeller, Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark
  • 9 J Holst, Department of Biomedcal Sciences, University of Copenhagen Faculty of Health and Medical Sciences, Kobenhavn, Denmark
  • 10 N Wewer Albrechtsen, Department of Biomedical Sciences, University of Copenhagen Faculty of Health and Medical Sciences, Kobenhavn, Denmark

Correspondence: Nicolai Wewer Albrechtsen, Email: nicolai.albrechtsen@sund.ku.dk

Objective: Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.

Design: Prospective longitudinal cohort study.

Materials and Methods: We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n=16), urosepsis (n=28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n=5). Correlations between C-Reactive Protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1ng/kg) in nine healthy young males.

Results: Glucagon and CRP were positively and significantly correlated (r=0.27; P=0.0003), whereas no significant association between GLP-1 and CRP was found (r=0.08, P=0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P<0.05) but not GLP-1.

Conclusions :Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.

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