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Association study of four variants in KCNQ1 with type 2 diabetes mellitus and premature coronary artery disease in a Chinese population

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Abstract

Four single nucleotide polymorphisms (SNPs, rs2237892, rs2237895, rs2237897, rs2283228) in KCNQ1 are associated with type 2 diabetes mellitus in different ancestral groups. We investigated whether these 4 genetic markers are determinants of type 2 diabetes and premature coronary artery disease (CAD) in a Chinese population. We studied 398 consecutive patients, including 180 with coronary stenosis ≥50% or previous myocardial infarction (male <55 years, female <65 years) and 218 controls without documented CAD. CAD cases and controls were genotyped for 4 SNPs by using the ligase detection reaction method. The 3 genotypes AA, AC, and CC were present in rs2283228 and rs2237895, and the 3 genotypes CC, CT, TT were present in rs2237897 and rs2237892. No differences were found in genotype distribution and allele frequencies of these 4 SNPs between subjects with and without type 2 diabetes. Logistic regression showed that the risk of premature CAD in subjects carrying the CC genotype at rs2237892 was reduced by 90% in relation to individuals carrying the TT genotype (OR = 0.100, 95% CI: 0.018–0.564, P = 0.009). The association of other 3 SNPs with premature CAD could not be detected, nor did there exist any association of these 4 SNPs among groups of patients with 0, 1, 2, and 3-vessel disease (all P > 0.05). Our data implicate rs2237892 in KCNQ1 as a protective gene variant against premature CAD and we couldn’t replicate any association of these 4 SNPs with T2DM or extent of coronary lesions in a Chinese population.

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Acknowledgments

This study was supported by grants from the Ministry of Education of P. R. China and the Nanjing Scientific Development Project (2006ZD016).

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Correspondence to Zhong Chen.

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Chen, Z., Zhang, X., Ma, G. et al. Association study of four variants in KCNQ1 with type 2 diabetes mellitus and premature coronary artery disease in a Chinese population. Mol Biol Rep 37, 207–212 (2010). https://doi.org/10.1007/s11033-009-9597-0

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  • DOI: https://doi.org/10.1007/s11033-009-9597-0

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