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TGF-β1 and incident type 2 diabetes Results from the MONICA/KORA case-cohort study, 1984–2002

  1. Christian Herder, PHD, MSC1,
  2. Astrid Zierer, PHD2,
  3. Wolfgang Koenig, MD (wolfgang.koenig{at}uniklinik-ulm.de)3,
  4. Michael Roden, MD1,4,
  5. Christa Meisinger, MD, MPH2 and
  6. Barbara Thorand, PHD, MPH2
  1. From the 1Institute of Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany
  2. the 2Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
  3. the 3Department of Internal Medicine II-Cardiology, University of Ulm Medical Center, Ulm, Germany; and
  4. the4Department of Medicine/Metabolic Diseases, Heinrich Heine University Düsseldorf, Düsseldorf, Germany

    Abstract

    Objective --- Subclinical inflammation leads to insulin resistance and β cell dysfunction. This study aimed to assess whether levels of circulating TGF-β1, a central, mainly immunosuppressive and anti-inflammatory cytokine, were associated with incident type 2 diabetes.

    Research Design and Methods --- We measured serum levels of TGF-β1 from 460 individuals with and 1,474 individuals without incident type 2 diabetes in a prospective case-cohort study within the population-based MONICA/KORA Augsburg cohort.

    Results --- Elevated TGF-β1 concentrations were associated with higher, not lower, risk for type 2 diabetes (age, sex and survey-adjusted HR (95%CI) for increasing TGF-β1 tertiles: 1.0; 1.08 (0.83–1.42); 1.41 (1.08–1.83); P(trend)=0.012). Adjustment for BMI, metabolic and lifestyle factors had virtually no impact on the effect size.

    Conclusions --- Elevated serum concentrations of the cytokine TGF-β1 indicate an increased risk for type 2 diabetes. TGF-β1 may be upregulated to counterbalance metabolic and immunological disturbances preceding type 2 diabetes.

    Footnotes

      • Received March 10, 2009.
      • Accepted July 3, 2009.
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