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Article: Adiponectin gene variants and the risk of coronary heart disease: a 16-year longitudinal study

TitleAdiponectin gene variants and the risk of coronary heart disease: a 16-year longitudinal study
Authors
Issue Date2014
PublisherBioScientifica Ltd. The Journal's web site is located at http://www.eje-online.org/
Citation
European Journal of Endocrinology, 2014, v. 171, p. 107-115 How to Cite?
AbstractOBJECTIVE: Circulating adiponectin levels have been shown to be associated with a risk of coronary heart disease (CHD). However, its primary role in protecting against the development of CHD remains controversial due to conflicting observations in prospective studies. To gain further insight into the primary role of adiponectin, our major objective was to investigate the relationship between single nucleotide polymorphisms (SNPs) of the adiponectin gene (ADIPOQ) and incident CHD in a population-based cohort with no CHD at baseline. DESIGN AND METHODS: We conducted a 16-year longitudinal study in 2196 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study (CRISPS). During 33 862 person-years of follow-up, 184 subjects developed CHD (cumulative incidence rate=5.4 per 1000 person-years). Nine ADIPOQ SNPs with potential functional relevance or shown to be associated with adiponectin levels and/or CHD were genotyped. RESULTS: Among the nine ADIPOQ SNPs, +276G>T (rs1501299) was independently associated with incident CHD in men but not in women, even after adjustments for traditional cardiovascular risk factors (Padjusted=5.5×10(-3) to 0.023; hazard ratio=1.39-1.54). Furthermore, there was a significant association of the T allele of +276G>T with a lower adiponectin level (P=0.027; β (95% CI)=-0.05 (-0.10, -0.01). CONCLUSIONS: This study demonstrated that +276G>T may be an independent predictor of CHD development. Our findings suggest that low adiponectin levels, as may be influenced by +276G>T, confer a higher risk of CHD, in keeping with a role of hypoadiponectinaemia in the development of CHD in the general population.
Persistent Identifierhttp://hdl.handle.net/10722/203086
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, CYYen_US
dc.contributor.authorHui, YLEen_US
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorWoo, YCen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorFong, HYen_US
dc.contributor.authorOng, KLen_US
dc.contributor.authorYeung, CYen_US
dc.contributor.authorJanus, EDen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorSham, PC-
dc.contributor.authorLam, KS-
dc.date.accessioned2014-09-19T11:29:49Z-
dc.date.available2014-09-19T11:29:49Z-
dc.date.issued2014en_US
dc.identifier.citationEuropean Journal of Endocrinology, 2014, v. 171, p. 107-115en_US
dc.identifier.urihttp://hdl.handle.net/10722/203086-
dc.description.abstractOBJECTIVE: Circulating adiponectin levels have been shown to be associated with a risk of coronary heart disease (CHD). However, its primary role in protecting against the development of CHD remains controversial due to conflicting observations in prospective studies. To gain further insight into the primary role of adiponectin, our major objective was to investigate the relationship between single nucleotide polymorphisms (SNPs) of the adiponectin gene (ADIPOQ) and incident CHD in a population-based cohort with no CHD at baseline. DESIGN AND METHODS: We conducted a 16-year longitudinal study in 2196 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study (CRISPS). During 33 862 person-years of follow-up, 184 subjects developed CHD (cumulative incidence rate=5.4 per 1000 person-years). Nine ADIPOQ SNPs with potential functional relevance or shown to be associated with adiponectin levels and/or CHD were genotyped. RESULTS: Among the nine ADIPOQ SNPs, +276G>T (rs1501299) was independently associated with incident CHD in men but not in women, even after adjustments for traditional cardiovascular risk factors (Padjusted=5.5×10(-3) to 0.023; hazard ratio=1.39-1.54). Furthermore, there was a significant association of the T allele of +276G>T with a lower adiponectin level (P=0.027; β (95% CI)=-0.05 (-0.10, -0.01). CONCLUSIONS: This study demonstrated that +276G>T may be an independent predictor of CHD development. Our findings suggest that low adiponectin levels, as may be influenced by +276G>T, confer a higher risk of CHD, in keeping with a role of hypoadiponectinaemia in the development of CHD in the general population.en_US
dc.languageengen_US
dc.publisherBioScientifica Ltd. The Journal's web site is located at http://www.eje-online.org/-
dc.relation.ispartofEuropean Journal of Endocrinologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleAdiponectin gene variants and the risk of coronary heart disease: a 16-year longitudinal studyen_US
dc.typeArticleen_US
dc.identifier.emailCheung, YY: cyy0219@hku.hken_US
dc.identifier.emailHui, YLE: eylhui@hku.hken_US
dc.identifier.emailCheung, BMY: mycheung@hku.hken_US
dc.identifier.emailWoo, YC: wooyucho@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailFong, HY: kalofong@hku.hken_US
dc.identifier.emailOng, KL: okl2000@hku.hken_US
dc.identifier.emailYeung, CY: ycy167@hku.hken_US
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_US
dc.identifier.authorityHui, YLE=rp01660en_US
dc.identifier.authorityCheung, BMY=rp01321en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.description.naturepostprint-
dc.identifier.doi10.1530/EJE-14-0079en_US
dc.identifier.pmid24760538-
dc.identifier.hkuros237154en_US
dc.identifier.hkuros230290-
dc.identifier.volume171en_US
dc.identifier.spage107en_US
dc.identifier.epage115en_US
dc.identifier.isiWOS:000338578000019-
dc.publisher.placeUnited Kingdom-

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