Association between DNA variant sites in the apolipoprotein A5 gene and coronary heart disease in Chinese

The recently discovered apolipoprotein A5 ( APOA5) gene has been shown to be important in determining plasma triglyceride levels, a major cardiovascular disease risk factor. We searched for possible associations of the APOA5 gene polymorphisms S19W and −1131T>C with coronary heart disease (CHD) i...

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Published inMetabolism, clinical and experimental Vol. 54; no. 5; pp. 568 - 572
Main Authors Liu, Hekun, Zhang, Sizhong, Lin, Jianyin, Li, Hai, Huang, Aimin, Xiao, Cuiying, Li, Xuefei, Su, Zhiguang, Wang, Chunting, Nebert, Daniel W., Zhou, Bing, Zheng, Keqin, Shi, Jiajun, Li, Guixin, Huang, Dejia
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.05.2005
Elsevier
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Summary:The recently discovered apolipoprotein A5 ( APOA5) gene has been shown to be important in determining plasma triglyceride levels, a major cardiovascular disease risk factor. We searched for possible associations of the APOA5 gene polymorphisms S19W and −1131T>C with coronary heart disease (CHD) in a Chinese population. A total of 483 Chinese CHD patients and 502 control non-CHD subjects were genotyped by polymerase chain reaction–restriction fragment length polymorphism for these 2 single nucleotide polymorphisms. We found that the minor allele 19W was observed only in CHD patients and not in controls, with allelic frequencies of 0.047 and 0.000, respectively ( P < .000001), and the minor allele −1131C was significantly higher in CHD patients than in controls (0.391 vs 0.299, P < .0001). These results suggest that both the S19W and −1131T>C variations in the APOA5 gene are associated with the CHD and appear to be 2 genetic risk factors for CHD susceptibility in Chinese. Moreover, we found that triglyceride levels were significantly higher in −1131C carriers than in −1131T subjects of the control group and that high-density–lipoprotein cholesterol was decreased in −1131C carriers among CHD patients.
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ISSN:0026-0495
1532-8600
DOI:10.1016/j.metabol.2004.11.009