File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Interleukin-6 receptor gene polymorphism modulates interleukin-6 levels and the metabolic syndrome: GBCS-CVD

TitleInterleukin-6 receptor gene polymorphism modulates interleukin-6 levels and the metabolic syndrome: GBCS-CVD
Authors
Issue Date2010
PublisherNorth American Association for the Study of Obesity. The Journal's web site is located at http://www.obesityresearch.org
Citation
Obesity, 2010, v. 18 n. 10, p. 1969-1974 How to Cite?
AbstractInterleukin-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. © 2010 The Obesity Society.
Persistent Identifierhttp://hdl.handle.net/10722/91488
ISSN
2015 Impact Factor: 3.614
2015 SCImago Journal Rankings: 2.016
ISI Accession Number ID
Funding AgencyGrant Number
NSFC/RGCHKU720/05
University of Hong Kong Foundation for Educational Development and Research, Hong Kong
Guangzhou Public Health Bureau and the Guangzhou Science and Technology Bureau, Guangzhou, China
University of Birmingham, UK
Funding Information:

The study is funded by an NSFC/RGC grant HKU720/05; The University of Hong Kong Foundation for Educational Development and Research, Hong Kong; the Guangzhou Public Health Bureau and the Guangzhou Science and Technology Bureau, Guangzhou, China; and The University of Birmingham, UK. The Guangzhou Biobank Cohort Study-CVD investigators include: the Guangzhou No. 12 Hospital: J.M.L., X.J.Y., B.L., C.Q.J. (Co-PI); The University of Hong Kong: T.H.L.; The Chinese University of Hong Kong: B. Tomlinson, K.S. Wong; The University of Birmingham: B.M.Y.C., G.N.T. (Co-PI).

References

 

DC FieldValueLanguage
dc.contributor.authorJiang, CQen_HK
dc.contributor.authorLam, THen_HK
dc.contributor.authorLiu, Ben_HK
dc.contributor.authorLin, JMen_HK
dc.contributor.authorYue, XJen_HK
dc.contributor.authorJin, YLen_HK
dc.contributor.authorCheung, BMYen_HK
dc.contributor.authorThomas, GNen_HK
dc.date.accessioned2010-09-17T10:20:13Z-
dc.date.available2010-09-17T10:20:13Z-
dc.date.issued2010en_HK
dc.identifier.citationObesity, 2010, v. 18 n. 10, p. 1969-1974en_HK
dc.identifier.issn1930-7381en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91488-
dc.description.abstractInterleukin-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. © 2010 The Obesity Society.en_HK
dc.languageengen_HK
dc.publisherNorth American Association for the Study of Obesity. The Journal's web site is located at http://www.obesityresearch.orgen_HK
dc.relation.ispartofObesityen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAllelesen_HK
dc.subject.meshBlood Glucose - metabolismen_HK
dc.subject.meshC-Reactive Protein - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFibrinogen - genetics - metabolismen_HK
dc.subject.meshGenetics, Populationen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInterleukin-6 - genetics - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMetabolic Syndrome X - epidemiology - genetics - metabolismen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolymorphism, Single Nucleotideen_HK
dc.subject.meshPrevalenceen_HK
dc.subject.meshReceptors, Interleukin-6 - genetics - metabolismen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshTriglycerides - blooden_HK
dc.titleInterleukin-6 receptor gene polymorphism modulates interleukin-6 levels and the metabolic syndrome: GBCS-CVDen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1930-7381&volume=18&issue=10&spage=1969&epage=1974&date=2010&atitle=Interleukin-6+receptor+gene+polymorphism+modulates+interleukin-6+levels+and+the+metabolic+syndrome:+GBCS-CVD-
dc.identifier.emailLam, TH:hrmrlth@hkucc.hku.hken_HK
dc.identifier.emailCheung, BMY:mycheung@hku.hken_HK
dc.identifier.authorityLam, TH=rp00326en_HK
dc.identifier.authorityCheung, BMY=rp01321en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/oby.2010.31en_HK
dc.identifier.pmid20186139-
dc.identifier.scopuseid_2-s2.0-77957105980en_HK
dc.identifier.hkuros180646-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957105980&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume18en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1969en_HK
dc.identifier.epage1974en_HK
dc.identifier.isiWOS:000282166800016-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridJiang, CQ=10639500500en_HK
dc.identifier.scopusauthoridLam, TH=7202522876en_HK
dc.identifier.scopusauthoridLiu, B=36079151900en_HK
dc.identifier.scopusauthoridLin, JM=35409737900en_HK
dc.identifier.scopusauthoridYue, XJ=35410971600en_HK
dc.identifier.scopusauthoridJin, YL=35558481400en_HK
dc.identifier.scopusauthoridCheung, BMY=7103294806en_HK
dc.identifier.scopusauthoridThomas, GN=35465269900en_HK
dc.identifier.citeulike8652728-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats