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Interleukin‐6 Receptor Gene Polymorphism Modulates Interleukin‐6 Levels and the Metabolic Syndrome: GBCS‐CVD
Author(s) -
Jiang Chao Qiang,
Lam Tai Hing,
Liu Bin,
Lin Jie Ming,
Yue Xiao Jun,
Jin Ya Li,
Cheung Bernard M.Y.,
Thomas G. Neil
Publication year - 2010
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2010.31
Subject(s) - single nucleotide polymorphism , genotype , medicine , endocrinology , snp , genotyping , interleukin , biology , gene , genetics , cytokine
Interleukin‐6 (IL‐6) is a key pleiotropic cytokine that modulates the inflammatory response. Single‐nucleotide polymorphisms (SNPs) within associated genes may contribute to the metabolic syndrome (MES). We examined the role of the IL‐6 (rs1524107‐C/T) and IL‐6 receptor (IL‐6R, rs8192284‐A/C, Asp358Ala) SNPs in modulating IL‐6 levels and the syndrome. A total of 1,979 older Chinese subjects aged 50–92 years from Guangzhou Biobank Cohort Study (GBCS) were recruited. SNPs were detected using Taqman SNP genotyping kits. IL‐6 was measured using enzyme‐linked immunosorbent assay. The genotype frequencies were 4.9, 33.9, and 61.3% for the IL‐6 CC, CT, and TT, and 12.0, 44.9, and 43.1% for the IL‐6R CC, AC, and AA, respectively. Both SNPs were in Hardy–Weinberg equilibrium. The IL‐6 SNP was not associated with IL‐6 levels or the MES, but was dose‐dependently associated with fibrinogen levels, P = 0.049. IL‐6 levels significantly decreased with increasing proportions of the IL‐6R A‐allele 9.8 ± 4.9, 9.3 ± 4.8, and 8.4 ± 4.3, respectively, P = 0.001. Conversely, the A‐allele was associated with elevated triglyceride, P = 0.009, C‐reactive protein, P = 0.047, and potentially with fasting glucose levels, P = 0.077. There was an increasing prevalence of the MES in those carrying the IL‐6R CC, AC, and AA genotypes at 18.1, 21.5, 25.2%, respectively, P = 0.010. The SNP was a significant independent predictor of the MES after adjusting for general obesity, age, gender and lifestyle, and socioeconomic parameters, P = 0.023. These data, which are in accord with studies from white populations suggest the IL‐6R SNP may play a role in the pathogenesis of the MES possibly through modulating IL‐6 levels.