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Huth, C. ; Heid, I.M. ; Vollmert, C. ; Gieger, C. ; Grallert, H. ; Wolford, J.K.* ; Langer, B. ; Thorand, B. ; Klopp, N. ; Hamid, Y.H.* ; Pedersen, O.* ; Hansen, T.* ; Lyssenko, V.* ; Groop, L.* ; Meisinger, C. ; Döring, A. ; Löwel, H. ; Lieb, W.* ; Hengstenberg, C.* ; Rathmann, W.* ; Martin, S.* ; Stephens, J.W.* ; Ireland, H.* ; Mather, H.* ; Miller, G.J.* ; Stringham, H.M.* ; Boehnke, M.* ; Tuomilehto, J.* ; Boeing, H.* ; Möhlig, M.* ; Spranger, J.* ; Pfeiffer, A.* ; Wernstedt, I.* ; Niklason, A.* ; Lopez-Bermejo, A.* ; Fernández-Real, J.M.* ; Hanson, R.L.* ; Gallart, L.* ; Vendrell, J.* ; Tsiavou, A.* ; Hatziagelaki, E.* ; Humphries, S.E.* ; Wichmann, H.-E. ; Herder, C.* ; Illig, T.

IL6 gene promoter polymorphisms and type 2 diabetes: Joint analysis of individual participants' data from 21 studies.

Diabetes 55, 2915-2921 (2006)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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20,000 participants from 21 published and unpublished studies.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. © 2006 by the American Diabetes Association.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Zeitschrift Diabetes
Quellenangaben Band: 55, Heft: 10, Seiten: 2915-2921 Artikelnummer: , Supplement: ,
Verlag American Diabetes Association
Verlagsort Alexandria, VA.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)