Diabetologia

, Volume 45, Issue 6, pp 805–812

Impaired glucose tolerance is associated with increased serum concentrations of interleukin 6 and co-regulated acute-phase proteins but not TNF-α or its receptors

  • S. Müller
  • S. Martin
  • W. Koenig
  • P. Hanifi-Moghaddam
  • W. Rathmann
  • B. Haastert
  • G. Giani
  • T. Illig
  • B. Thorand
  • H. Kolb
Article

DOI: 10.1007/s00125-002-0829-2

Cite this article as:
Müller, S., Martin, S., Koenig, W. et al. Diabetologia (2002) 45: 805. doi:10.1007/s00125-002-0829-2

Abstract

Aims/hypothesis. A population-based sample was studied to define immune abnormalities in individuals at risk of Type II (non-insulin-dependent) diabetes mellitus because of impaired glucose tolerance.

Methods. A total of 1653 individuals aged 55 to 74 years participated in a population based survey in Southern Germany (KORA Survey 2000). Those without a history of diabetes were subjected to an OGTT. Randomly selected subjects with IGT (n=80) were compared with non-diabetic control subjects (n=77) and patients with Type II diabetes (n=152) of the same population-based sample after matching for age and sex. Immune parameters were analysed in serum with rigidly evaluated ELISA.

Results. Serum pro-inflammatory cytokine interleukin 6 (IL-6) concentrations were higher in subjects with IGT and Type II diabetes than in the control subjects (median 1.8 and 2.5 vs 0.8 pg/ml, p<0.0001). Soluble IL-6 receptors potentiate IL-6 bioactivity and their concentrations were mildly increased in Type II diabetes (p<0.05). These immune changes seem relevant because IL-6 dependent acute-phase proteins C-reactive protein, serum amyloid A protein and fibrinogen were also increased in IGT and Type II diabetes. Circulating concentrations of TNF-α and its two receptors sTNF-R60 and sTNF-R80 were not increased in IGT subjects compared with the control subjects.

Conclusion/interpretation. Our study shows systemic up-regulation of selected inflammatory mediators in patients with Type II diabetes and IGT. The pattern observed is non-random and fits with an IL-6 associated rather than TNF-α associated response.

Type II diabetes impaired glucose tolerance systemic inflammation interleukin 6 tumour necrosis factor α C-reactive protein serum amyloid A protein innate immunity cytokine acute-phase protein
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Copyright information

© Springer-Verlag 2002

Authors and Affiliations

  • S. Müller
    • 1
  • S. Martin
    • 1
  • W. Koenig
    • 2
  • P. Hanifi-Moghaddam
    • 1
  • W. Rathmann
    • 3
  • B. Haastert
    • 3
  • G. Giani
    • 3
  • T. Illig
    • 4
  • B. Thorand
    • 4
  • H. Kolb
    • 1
  1. 1.German Diabetes Clinic, German Diabetes Research Institute at the University of Düsseldorf, Auf'm Hennekamp 65, DüsseldorfGermany
  2. 2.Department Internal Medicine II-Cardiology, University of Ulm, Medical Center, UlmGermany
  3. 3.Department of Biometrics and Epidemiology, German Diabetes Research Institute at the University of Düsseldorf, DüsseldorfGermany
  4. 4.National Research Center for Environment and Health, Institute of Epidemiology, NeuherbergGermany