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Diabetes 52:812-817, 2003
© 2003 by the American Diabetes Association, Inc.

Inflammatory Cytokines and the Risk to Develop Type 2 Diabetes

Results of the Prospective Population-Based European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study

Joachim Spranger1,2, Anja Kroke3, Matthias Möhlig1,2, Kurt Hoffmann3, Manuela M. Bergmann3, Michael Ristow1,2, Heiner Boeing3, and Andreas F.H. Pfeiffer1,2

1 Department of Endocrinology, Diabetes and Nutrition, Benjamin Franklin Medical Center, Free University Berlin, Berlin, Germany
2 Department of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, Potsdam-Rehbrücke, Germany
3 Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Potsdam-Rehbrücke, Germany

A subclinical inflammatory reaction has been shown to precede the onset of type 2 (non-insulin-dependent) diabetes. We therefore examined prospectively the effects of the central inflammatory cytokines interleukin (IL)-1ß, IL-6, and tumor necrosis factor-{alpha} (TNF-{alpha}) on the development of type 2 diabetes. We designed a nested case-control study within the prospective population-based European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study including 27,548 individuals. Case subjects were defined to be those who were free of type 2 diabetes at baseline and subsequently developed type 2 diabetes during a 2.3-year follow-up period. A total of 192 cases of incident type 2 diabetes were identified and matched with 384 non-disease-developing control subjects. IL-6 and TNF-{alpha} levels were found to be elevated in participants with incident type 2 diabetes, whereas IL-1ß plasma levels did not differ between the groups. Analysis of single cytokines revealed IL-6 as an independent predictor of type 2 diabetes after adjustment for age, sex, BMI, waist-to-hip ratio (WHR), sports, smoking status, educational attainment, alcohol consumption, and HbA1c (4th vs. the 1st quartile: odds ratio [OR] 2.6, 95% CI 1.2–5.5). The association between TNF-{alpha} and future type 2 diabetes was no longer significant after adjustment for BMI or WHR. Interestingly, combined analysis of the cytokines revealed a significant interaction between IL-1ß and IL-6. In the fully adjusted model, participants with detectable levels of IL-1ß and elevated levels of IL-6 had an independently increased risk to develop type 2 diabetes (3.3, 1.7–6.8), whereas individuals with increased concentrations of IL-6 but undetectable levels of IL-1ß had no significantly increased risk, both compared with the low-level reference group. These results were confirmed in an analysis including only individuals with HbA1c <5.8% at baseline. Our data suggest that the pattern of circulating inflammatory cytokines modifies the risk for type 2 diabetes. In particular, a combined elevation of IL-1ß and IL-6, rather than the isolated elevation of IL-6 alone, independently increases the risk of type 2 diabetes. These data strongly support the hypothesis that a subclinical inflammatory reaction has a role in the pathogenesis of type 2 diabetes.


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