Anne Juhl

Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review


  • bcp.14063

    Forlagets udgivne version, 881 KB, PDF-dokument


  • Christina Brock
  • Christian Stevns Hansen, Steno Diabetes Center
  • ,
  • Jesper Karmisholt, Steno Diabetes Center North, Aalborg Universitet
  • ,
  • Holger Jon Møller
  • Anne Juhl
  • Adam Donald Farmer, Queen Mary University of London, University Hospital of North Staffordshire NHS Trust
  • ,
  • Asbjørn Mohr Drewes
  • Sam Riahi, Aalborg Universitet
  • ,
  • Hans Henrik Lervang, Københavns Universitet
  • ,
  • Poul Erik Jakobsen
  • Birgitte Brock, Steno Diabetes Center

Aims: Type 1 diabetes can be complicated with neuropathy that involves immune-mediated and inflammatory pathways. Glucagon-like peptide-1 receptor agonists such as liraglutide, have shown anti-inflammatory properties, and thus we hypothesized that long-term treatment with liraglutide induced diminished inflammation and thus improved neuronal function. Methods: The study was a randomized, double-blinded, placebo-controlled trial of adults with type 1 diabetes and confirmed symmetrical polyneuropathy. They were randomly assigned (1:1) to receive either liraglutide or placebo. Titration was 6 weeks to 1.2–1.8 mg/d, continuing for 26 weeks. The primary endpoint was change in latency of early brain evoked potentials. Secondary endpoints were changes in proinflammatory cytokines, cortical evoked potential, autonomic function and peripheral neurophysiological testing. Results: Thirty-nine patients completed the study, of whom 19 received liraglutide. In comparison to placebo, liraglutide reduced interleukin-6 (−22.6%; 95% confidence interval [CI]: −38.1, −3.2; P =.025) with concomitant numerical reductions in other proinflammatory cytokines. However neuronal function was unaltered at the central, autonomic or peripheral level. Treatment was associated with −3.38 kg (95% CI: −5.29, −1.48; P <.001] weight loss and a decrease in urine albumin/creatinine ratio (−40.2%; 95% CI: −60.6, −9.5; P =.02). Conclusion: Hitherto, diabetic neuropathy has no cure. Speculations can be raised whether mechanism targeted treatment, e.g. lowering the systemic level of proinflammatory cytokines may lead to prevention or treatment of the neuroinflammatory component in early stages of diabetic neuropathy. If ever successful, this would serve as an example of how fundamental mechanistic principles are translated into clinical practice similar to those applied in the cardiovascular and nephrological clinic.

TidsskriftBritish Journal of Clinical Pharmacology
Sider (fra-til)2512-2523
Antal sider12
StatusUdgivet - 2019

Se relationer på Aarhus Universitet Citationsformater

ID: 172164463