• Media type: E-Article
  • Title: IL6 Gene Promoter Polymorphisms and Type 2 Diabetes
  • Contributor: Huth, Cornelia; Heid, Iris M.; Vollmert, Caren; Gieger, Christian; Grallert, Harald; Wolford, Johanna K.; Langer, Birgit; Thorand, Barbara; Klopp, Norman; Hamid, Yasmin H.; Pedersen, Oluf; Hansen, Torben; Lyssenko, Valeriya; Groop, Leif; Meisinger, Christa; Döring, Angela; Löwel, Hannelore; Lieb, Wolfgang; Hengstenberg, Christian; Rathmann, Wolfgang; Martin, Stephan; Stephens, Jeffrey W.; Ireland, Helen; Mather, Hugh; [...]
  • imprint: American Diabetes Association, 2006
  • Published in: Diabetes
  • Language: English
  • DOI: 10.2337/db06-0600
  • ISSN: 0012-1797; 1939-327X
  • Keywords: Endocrinology, Diabetes and Metabolism ; Internal Medicine
  • Origination:
  • Footnote:
  • Description: <jats:p>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&amp;gt;C (rs1800795) and −573G&amp;gt;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two IL6 variants and type 2 diabetes, we analyzed individual data on &amp;gt;20,000 participants from 21 published and unpublished studies.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&amp;gt;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&amp;gt;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.</jats:p>
  • Access State: Open Access