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      Single nucleotide polymorphism rs3774261 in the AdipoQ gene is associated with the risk of coronary heart disease (CHD) in Northeast Han Chinese population: a case-control study

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          Abstract

          Background

          Coronary Heart Disease (CHD) is one of the leading causes of death in the world with a projected global 82 million DALYs by 2020. Genetic and environmental factors contribute to CHD development. Here, the authors investigate the association between CHD risk and three Single Nucleotide Polymorphisms (SNPs) in the AdipoQ gene (rs3774261, rs1063537 and rs2082940); and the interaction of this association with environmental factors, in Northeast Han Chinese population.

          Methods

          Using a case–control study design, 1514 participants (754 cases and 760 controls) were investigated. Three variants in the AdipoQ gene (rs3774261, rs1063537 and rs2082940) were selected and genotyped. The online SNPstats program and SPSS 21.0 software were used for data analyses.

          Results

          The authors found that the rs3774261G allele is associated with the risk of CHD but that the rs2082940T allele protects against CHD. No significant association was found between rs1063537 and CHD risk. The study also found significant interactions between triglyceride levels and the SNPs studied ( P < 0.0001 for rs3774261, P = 0.014 for rs1063537, and P = 0.031 for rs2082940).

          Conclusions

          Variations in AdipoQ gene can protect against CHD (as with rs2082940T) or associated with CHD risk (as with rs3774261G) in Northeast Han Chinese – findings that will help shed light on the reported conflicting roles of AdipoQ in cardiovascular diseases. Serum triglycerides levels also interact in the AdipoQ – CHD association, thus further highlighting the roles environmental factors play in the genetic aspect of diseases.

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          Most cited references64

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          Pathophysiology of coronary artery disease.

          During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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            cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (AdiPose Most abundant Gene transcript 1).

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              Plasma adiponectin levels and risk of myocardial infarction in men.

              Adiponectin, a recently discovered adipocyte-derived peptide, is involved in the regulation of insulin sensitivity and lipid oxidation and, purportedly, in the development of atherosclerosis and coronary heart disease in humans. To assess prospectively whether plasma adiponectin concentrations are associated with risk of myocardial infarction (MI). Nested case-control study among 18 225 male participants of the Health Professionals Follow-up Study aged 40 to 75 years who were free of diagnosed cardiovascular disease at the time of blood draw (1993-1995). During 6 years of follow-up through January 31, 2000, 266 men subsequently developed nonfatal MI or fatal coronary heart disease. Using risk set sampling, controls were selected in a 2:1 ratio matched for age, date of blood draw, and smoking status (n = 532). Incidence of nonfatal MI and fatal coronary heart disease by adiponectin level. After adjustment for matched variables, participants in the highest compared with the lowest quintile of adiponectin levels had a significantly decreased risk of MI (relative risk [RR], 0.39; 95% confidence interval [CI], 0.23-0.64; P for trend <.001). Additional adjustment for family history of MI, body mass index, alcohol consumption, physical activity, and history of diabetes and hypertension did not substantively affect this relationship (RR, 0.41; 95% CI, 0.24-0.70; P for trend <.001). Further adjustment for hemoglobin A1c or C-reactive protein levels also had little impact, but additional adjustment for low- and high-density lipoprotein cholesterol levels modestly attenuated this association (RR, 0.56; 95% CI, 0.32-0.99; P for trend =.02). High plasma adiponectin concentrations are associated with lower risk of MI in men. This relationship can be only partly explained by differences in blood lipids and is independent of inflammation and glycemic status.
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                Author and article information

                Contributors
                samjokanu@yahoo.com
                gyluisme@163.com
                13514303555@163.com
                1076158138@qq.com
                810456330@qq.com
                1840128897@qq.com
                15843100951@qq.com
                l_yong@jlu.edu.cn
                yuyaqin5540@163.com
                +86-431-85619419 , chengyi@jlu.edu.cn
                +86-431-85619419 , ywliu@jlu.edu.cn
                Journal
                Lipids Health Dis
                Lipids Health Dis
                Lipids in Health and Disease
                BioMed Central (London )
                1476-511X
                12 January 2016
                12 January 2016
                2016
                : 15
                : 6
                Affiliations
                [ ]Department of Epidemiology and Biostatistics, School of Public Health of Jilin University, Changchun, 130021 China
                [ ]Clinical laboratory of China-Japan Union Hospital of Jilin University, Changchun, China
                [ ]The General Hospital of Jilin Chemical Group Corporation, Jilin, 132022 China
                [ ]The Cardiovascular Center, the First Hospital of Jilin University, Changchun, 130021 China
                Author information
                http://orcid.org/0000-0003-2859-4771
                Article
                173
                10.1186/s12944-015-0173-4
                4709904
                26754433
                87012573-55eb-4b03-9eec-6002ceaa6004
                © Kanu et al. 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 15 November 2015
                : 29 December 2015
                Funding
                Funded by: The National Natural Science Foundation of China
                Award ID: Grant 81573230
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Biochemistry
                adipoq,adiponectin,polymorphism,coronary heart disease,risk,association,interaction
                Biochemistry
                adipoq, adiponectin, polymorphism, coronary heart disease, risk, association, interaction

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