Targeting gp130 to prevent inflammation and promote insulin action

M J Kraakman, T L Allen, M Whitham, P Iliades, H L Kammoun, E Estevez, G I Lancaster, M A Febbraio

Research output: Contribution to journalReview articlepeer-review

21 Citations (Scopus)


Obesity and type 2 diabetes are now the most prevalent metabolic diseases in the Western world and the development of new strategies to treat these metabolic diseases is most warranted. Obesity results in a state of chronic low-grade inflammation in metabolically active tissues such as the liver, adipose tissue, brain and skeletal muscle. Work in our laboratory has focussed on the role of the cytokine interleukin-6 (IL)-6 and other IL-6-like cytokines that signal through the gp130 receptor complex. We have focussed on the role of blocking IL-6 trans-signalling to prevent inflammation on the one hand, and activating membrane-bound signalling to promote insulin sensitivity on the other hand. Since the cloning of the IL-6 gene nearly 30  years ago, a pattern has emerged associating IL-6 with a number of diseases associated with inflammation including rheumatoid arthritis (RA), Crohn's disease and several cancers. Accordingly, tocilizumab, an IL-6 receptor-inhibiting monoclonal antibody, is now useful for the treatment of RA. However, this may not be the most optimal strategy to block inflammation associated with IL-6 and may result in unwanted side effects that, paradoxically, could actually promote metabolic disease.

Original languageEnglish
Pages (from-to)170-5
Number of pages6
JournalDiabetes, obesity & metabolism
Volume15 Suppl 3
Publication statusPublished - Sept 2013
Externally publishedYes


  • Animals
  • Antibodies, Monoclonal, Humanized/therapeutic use
  • Cytokine Receptor gp130/antagonists & inhibitors
  • Humans
  • Inflammation/prevention & control
  • Insulin/physiology
  • Insulin Resistance/physiology
  • Interleukin-6/physiology
  • Molecular Targeted Therapy
  • Obesity/complications
  • Signal Transduction


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