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

Huth, Cornelia ; Heid, Iris M. ; Vollmert, Caren ; Gieger, Christian ; Grallert, Harald ; Wolford, Johanna K. ; Langer, Birgit ; Thorand, Barbara ; Klopp, Norman and Hamid, Yasmin H. , et al. (2006) In Diabetes 55(10). p.2915-2921
Abstract
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 20,000 participants from 21 published and unpublished studies.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... (More)
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 20,000 participants from 21 published and unpublished studies.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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes
volume
55
issue
10
pages
2915 - 2921
publisher
American Diabetes Association Inc.
external identifiers
  • wos:000240910400033
  • pmid:17003362
  • scopus:33750877102
ISSN
1939-327X
DOI
10.2337/db06-0600
language
English
LU publication?
yes
id
1bad217c-126e-4578-9823-8459abfbaadf (old id 686024)
date added to LUP
2016-04-01 15:50:44
date last changed
2020-09-27 05:31:44
@article{1bad217c-126e-4578-9823-8459abfbaadf,
  abstract     = {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.},
  author       = {Huth, Cornelia and Heid, Iris M. and Vollmert, Caren and Gieger, Christian and Grallert, Harald and Wolford, Johanna K. and Langer, Birgit and Thorand, Barbara and Klopp, Norman and Hamid, Yasmin H. and Pedersen, Oluf and Hansen, Torben and Lyssenko, Valeriya and Groop, Leif and Meisinger, Christa and Doring, Angela and Lowel, Hannelore and Lieb, Wolfgang and Hengstenberg, Christian and Rathmann, Wolfgang and Martin, Stephan and Stephens, Jeffrey W. and Ireland, Helen and Mather, Hugh and Miller, George J. and Stringham, Heather M. and Boehnke, Michael and Tuomilehto, Jaakko and Boeing, Heiner and Mohlig, Matthias and Spranger, Joachim and Pfeiffer, Andreas and Wernstedt, Ingrid and Niklason, Anders and Lopez-Bermejo, Abel and Fernandez-Real, Jose-Manuel and Hanson, Robert L. and Gallart, Luis and Vendrell, Joan and Tsiavou, Anastasia and Hatziagelaki, Erifili and Humphries, Steve E. and Wichmann, H. -Erich and Herder, Christian and Illig, Thomas},
  issn         = {1939-327X},
  language     = {eng},
  number       = {10},
  pages        = {2915--2921},
  publisher    = {American Diabetes Association Inc.},
  series       = {Diabetes},
  title        = {IL6 gene promoter polymorphisms and type 2 diabetes - Joint analysis of individual participants' data from 21 studies},
  url          = {http://dx.doi.org/10.2337/db06-0600},
  doi          = {10.2337/db06-0600},
  volume       = {55},
  year         = {2006},
}