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Conference Paper: Adiponectin gene polymorphisms, plasma adiponectin concentration and persistent hypertension in Hong Kong Chinese

TitleAdiponectin gene polymorphisms, plasma adiponectin concentration and persistent hypertension in Hong Kong Chinese
Authors
Issue Date2009
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCP
Citation
The 2009 Meeting of the Clinical Pharmacology Section of the British Pharmacological Society, London, UK., 15-17 December 2009. In British Journal of Clinical Pharmacology, 2009, v. 70 n. 2, p. 303 How to Cite?
AbstractLow plasma adiponectin concentrations can predict the development of hypertension after 5 years in our population. We therefore investigated if single nucleotide polymorphisms (SNPs) in the adiponectin gene influenced plasma adiponectin concentrations and whether they were associated with hypertension. We genotyped 14 tagging SNPs in 1936 subjects, from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2). Plasma adiponectin concentrations were measured in 1650 subjects. Among the 14 SNPs, rs266729 (b = -0.071, P = 0.0008), -10677C > T (b = 0.067, P = 0.0017), rs182052 (b = -0.095, P < 0.0001) and rs12495941 (b = 0.100, P < 0.0001) were significantly associated with adiponectin concentrations after adjusting for covariates. Among all the 1936 subjects, none of the SNPs was significantly associated with prevalent and incident hypertension. However, in the sub-cohort of 1616 subjects who were consistently normotensive or hypertensive at baseline and follow-up, the minor G allele of the SNP rs266729 was significantly associated with a higher odds of hypertension (odds ratio [95%CI] = 1.49 [1.13, 1.95], P = 0.0044) after adjusting for covariates. In stepwise multiple logistic regression, this SNP (P = 0.020) was a significant independent factor of hypertension, together with age (P < 0.001), body mass index (P < 0.001), triglycerides (P =0.020) and HOMA-IR (P < 0.001). No significant sex-interaction was found for the SNPs with adiponectin concentration and hypertension. Similar results were obtained in haplotype analysis. In our population, genetic variants in the adiponectin gene influenced plasma adiponectin concentrations. As SNP 266729 was associated with persistent hypertension in this population, further studies on the genetic association of adiponectin with hypertension are warranted.
DescriptionThis journal issue contains Proceedings of the BPS Clinical Pharmacological Section
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/143673
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 1.046

 

DC FieldValueLanguage
dc.contributor.authorOng, KLen_US
dc.contributor.authorLi, Men_US
dc.contributor.authorTso, AWKen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorCherny, SSen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2011-12-16T08:09:21Z-
dc.date.available2011-12-16T08:09:21Z-
dc.date.issued2009en_US
dc.identifier.citationThe 2009 Meeting of the Clinical Pharmacology Section of the British Pharmacological Society, London, UK., 15-17 December 2009. In British Journal of Clinical Pharmacology, 2009, v. 70 n. 2, p. 303en_US
dc.identifier.issn0306-5251en_US
dc.identifier.urihttp://hdl.handle.net/10722/143673-
dc.descriptionThis journal issue contains Proceedings of the BPS Clinical Pharmacological Section-
dc.descriptionOpen Access Journal-
dc.description.abstractLow plasma adiponectin concentrations can predict the development of hypertension after 5 years in our population. We therefore investigated if single nucleotide polymorphisms (SNPs) in the adiponectin gene influenced plasma adiponectin concentrations and whether they were associated with hypertension. We genotyped 14 tagging SNPs in 1936 subjects, from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2). Plasma adiponectin concentrations were measured in 1650 subjects. Among the 14 SNPs, rs266729 (b = -0.071, P = 0.0008), -10677C > T (b = 0.067, P = 0.0017), rs182052 (b = -0.095, P < 0.0001) and rs12495941 (b = 0.100, P < 0.0001) were significantly associated with adiponectin concentrations after adjusting for covariates. Among all the 1936 subjects, none of the SNPs was significantly associated with prevalent and incident hypertension. However, in the sub-cohort of 1616 subjects who were consistently normotensive or hypertensive at baseline and follow-up, the minor G allele of the SNP rs266729 was significantly associated with a higher odds of hypertension (odds ratio [95%CI] = 1.49 [1.13, 1.95], P = 0.0044) after adjusting for covariates. In stepwise multiple logistic regression, this SNP (P = 0.020) was a significant independent factor of hypertension, together with age (P < 0.001), body mass index (P < 0.001), triglycerides (P =0.020) and HOMA-IR (P < 0.001). No significant sex-interaction was found for the SNPs with adiponectin concentration and hypertension. Similar results were obtained in haplotype analysis. In our population, genetic variants in the adiponectin gene influenced plasma adiponectin concentrations. As SNP 266729 was associated with persistent hypertension in this population, further studies on the genetic association of adiponectin with hypertension are warranted.-
dc.languageeng-
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCPen_US
dc.relation.ispartofBritish Journal of Clinical Pharmacologyen_US
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.titleAdiponectin gene polymorphisms, plasma adiponectin concentration and persistent hypertension in Hong Kong Chineseen_US
dc.typeConference_Paperen_US
dc.identifier.emailOng, KL: okl2000@hku.hken_US
dc.identifier.emailLi, M: mingflee@hotmail.com-
dc.identifier.emailTso, AWK: awktso@hku.hk-
dc.identifier.emailXu, A: amxu@hku.hk-
dc.identifier.emailCherny, SS: cherny@hku.hk-
dc.identifier.emailSham, PC: pcsham@.hku.hk-
dc.identifier.emailTse, HF: hftse@hku.hk-
dc.identifier.emailCheung, BMY: mycheung@hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.authorityTso, AWK=rp00535en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1365-2125.2010.03678.x-
dc.identifier.hkuros168893-
dc.identifier.hkuros188445-
dc.identifier.volume70en_US
dc.identifier.issue2-
dc.identifier.spage303en_US
dc.identifier.epage303en_US
dc.publisher.placeUnited Kingdom-
dc.description.otherMeeting of the Clinical Pharmacology Section of the British-Pharmacological-Society, London, UK., 15-17 December 2009. In British Journal of Clinical Pharmacology, 2009, v. 70 n. 2, p. 303-
dc.customcontrol.immutablesml 161216 - merged-
dc.identifier.issnl0306-5251-

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