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Conference Paper: Role of genetic variants in gene encoding lipocalin-2 in the development of elevated blood pressure

TitleRole of genetic variants in gene encoding lipocalin-2 in the development of elevated blood pressure
Authors
Issue Date2011
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk
Citation
The 16th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, China, 22 January 2011. In the Hong Kong Medical Journal, 2011, v. 17 n. 1, Suppl. 1, p. 17, abstract no. 15 How to Cite?
AbstractIntroduction: Lipocalin-2 is recently recognised as a biomarker of obesity and inflammation, which are both risk factors for hypertension. We therefore investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding lipocalin-2 (LCN2) with elevated blood pressure in Hong Kong Chinese. Methods: Five tagging SNPs were genotyped in 1936 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) with a median follow-up period of 6.4 years. Elevated blood pressure was defined as ≥130/85 mm Hg or taking anti-hypertensive medication. Results: There were only two haplotypes with frequency of >5%, namely AGATC (45.5%) and GGTCC (41.2%). Haplotype GGTCC was associated with elevated blood pressure at follow-up (OR=1.17 compared to haplotype AGATC, P=0.031 after adjusting for age and sex). Among 1381 subjects without elevated blood pressure at baseline, 321 subjects developed elevated blood pressure at follow-up. Haplotype GGTCC was associated with the development of elevated blood pressure at follow-up (OR=1.30 compared to haplotype AGATC, P=0.011 after adjusting for age, sex, systolic blood pressure, and follow-up duration; OR=1.44, P=0.0015 after further adjusting for other covariates). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher systolic blood pressure than non-carriers (119.7±16.4 mm Hg vs 117.9±17.3 mm Hg, P=0.043). Conclusion: Our findings suggest, for the first time, that genetic variants in LCN2 may affect blood pressure. Further studies on the role of lipocalin-2 in blood pressure regulation are warranted. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/140170
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorOng, KLen_US
dc.contributor.authorTso, AWKen_US
dc.contributor.authorCherny, SSen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorLam, THen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2011-09-23T06:08:05Z-
dc.date.available2011-09-23T06:08:05Z-
dc.date.issued2011en_US
dc.identifier.citationThe 16th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, China, 22 January 2011. In the Hong Kong Medical Journal, 2011, v. 17 n. 1, Suppl. 1, p. 17, abstract no. 15en_US
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/140170-
dc.description.abstractIntroduction: Lipocalin-2 is recently recognised as a biomarker of obesity and inflammation, which are both risk factors for hypertension. We therefore investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding lipocalin-2 (LCN2) with elevated blood pressure in Hong Kong Chinese. Methods: Five tagging SNPs were genotyped in 1936 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) with a median follow-up period of 6.4 years. Elevated blood pressure was defined as ≥130/85 mm Hg or taking anti-hypertensive medication. Results: There were only two haplotypes with frequency of >5%, namely AGATC (45.5%) and GGTCC (41.2%). Haplotype GGTCC was associated with elevated blood pressure at follow-up (OR=1.17 compared to haplotype AGATC, P=0.031 after adjusting for age and sex). Among 1381 subjects without elevated blood pressure at baseline, 321 subjects developed elevated blood pressure at follow-up. Haplotype GGTCC was associated with the development of elevated blood pressure at follow-up (OR=1.30 compared to haplotype AGATC, P=0.011 after adjusting for age, sex, systolic blood pressure, and follow-up duration; OR=1.44, P=0.0015 after further adjusting for other covariates). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher systolic blood pressure than non-carriers (119.7±16.4 mm Hg vs 117.9±17.3 mm Hg, P=0.043). Conclusion: Our findings suggest, for the first time, that genetic variants in LCN2 may affect blood pressure. Further studies on the role of lipocalin-2 in blood pressure regulation are warranted. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.-
dc.languageengen_US
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk-
dc.relation.ispartofHong Kong Medical Journalen_US
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleRole of genetic variants in gene encoding lipocalin-2 in the development of elevated blood pressureen_US
dc.typeConference_Paperen_US
dc.identifier.emailCheung, BMY: mycheung@hku.hken_US
dc.identifier.emailOng, KL: okl2000@hku.hken_US
dc.identifier.emailTso, AWK: awktso@hku.hken_US
dc.identifier.emailCherny, SS: cherny@hku.hken_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.authorityCheung, BMY=rp01321en_US
dc.identifier.authorityTso, AWK=rp00535en_US
dc.identifier.authorityCherny, SS=rp00232en_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.identifier.authorityLam, TH=rp00326en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros194406en_US
dc.identifier.volume17-
dc.identifier.issue1, Suppl. 1-
dc.identifier.spage17, abstract no. 15-
dc.identifier.epage17, abstract no. 15-
dc.publisher.placeHong Kong-

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