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IL6 Gene Promoter Polymorphisms and Type 2 Diabetes

Joint Analysis of Individual Participants’ Data From 21 Studies

¹ GSF-Institute of Epidemiology, Neuherberg, Germany
² Institute of Biometry and Epidemiology, University of Munich, Munich, Germany
³ Translational Genomics Research Institute, Phoenix, Arizona
⁴ Steno Diabetes Center, Copenhagen, Denmark
⁵ Department of Clinical Sciences, University Hospital Malmö, Malmö, Sweden
⁶ Clinic and Policlinic for Internal Medicine II and Institute of Human Genetics, University of Lübeck, Lübeck, Germany
⁷ Clinic and Policlinic for Internal Medicine II, University of Regensburg, Regensburg, Germany
⁸ German Diabetes Center, Leibniz Institute at Heinrich Heine University Düsseldorf, Düsseldorf, Germany
⁹ Medical School, University of Wales, Swansea, U.K
¹⁰ Centre for Cardiovascular Genetics, Royal Free and University College Medical School, London, U.K
¹¹ Ealing Hospital, London, U.K
¹² Medical Research Council Cardiovascular Research Group, Wolfson Institute of Preventive Medicine, London, U.K
¹³ Department of Biostatistics, University of Michigan, Ann Arbor, Michigan
¹⁴ Diabetes and Genetic Epidemiology Unit, National Public Health Institute, Helsinki, Finland
¹⁵ Department of Public Health, University of Helsinki, Helsinki, Finland
¹⁶ South Ostrobothnia Central Hospital, Seinäjoki, Finland
¹⁷ Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
¹⁸ Department of Clinical Nutrition, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
¹⁹ Institute of Neuroscience and Physiology, Sahlgrenska Academy at Gothenborg University, Gothenborg, Sweden
²⁰ Department of Clinical Pharmacology, Sahlgrenska University Hospital, Gothenburg, Sweden
²¹ Diabetes, Endocrinology and Nutrition Unit, University Hospital Josep Trueta, Girona, Spain
²² National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, Arizona
²³ Research Unit, University Hospital Joan XXIII, Tarragona, Spain
²⁴ Onassis Cardiac Surgery Center, Molecular Immunopathology and Histocompatibility Laboratory, Athens, Greece
²⁵ 2nd Department of Internal Medicine, University Hospital Attikon, Athens, Greece

Address correspondence and reprint requests to Dr. Thomas Illig, Institute of Epidemiology, GSF-National Research Center for Environment and Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany. E-mail: illig{at}gsf.de

Abbreviations: FHS, Framingham Heart Study; HWE, Hardy-Weinberg equilibrium; IL, interleukin; IPD, individual participants’ data

Several lines of evidence indicate a causal role of the cytokine interleukin (IL)-6 in the development of type 2 diabetes in humans. Two common polymorphisms in the promoter of the IL-6 encoding gene IL6, –174G>C (rs1800795) and –573G>C (rs1800796), have been investigated for association with type 2 diabetes in numerous studies but with results that have been largely equivocal. To clarify the relationship between the two IL6 variants and type 2 diabetes, we analyzed individual data on >20,000 participants from 21 published and unpublished studies. Collected data represent eight different countries, making this the largest association analysis for type 2 diabetes reported to date. The GC and CC genotypes of IL6 –174G>C were associated with a decreased risk of type 2 diabetes (odds ratio 0.91, P = 0.037), corresponding to a risk modification of nearly 9%. No evidence for association was found between IL6 –573G>C and type 2 diabetes. The observed association of the IL6 –174 C-allele with a reduced risk of type 2 diabetes provides further evidence for the hypothesis that immune mediators are causally related to type 2 diabetes; however, because the association is borderline significant, additional data are still needed to confirm this finding.

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