Lack of association between genetic polymorphisms within DUSP12 -ATF6locus and glucose metabolism related traits in a Chinese population

BMC Medical Genetics

Research Article

Cheng Hu¹  Jie Wang¹  Rong Zhang¹  Yuqian Bao¹  Weiping Jia¹  Xiaojing Ma¹  Kunsan Xiang¹  Congrong Wang¹ 

[1] Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, P.R. China;

关键词: Endoplasmic Reticulum Stress;    Unfold Protein Response;    Normal Glucose Regulation;    Additive Model Adjust;    Shanghai Diabetes Study;   

DOI  :  10.1186/1471-2350-12-3

 received in 2010-07-16, accepted in 2011-01-06,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundGenome-wide linkage studies in multiple ethnic populations found chromosome 1q21-q25 was the strongest and most replicable linkage signal in the human chromosome. Studies in Pima Indian, Caucasians and African Americans identified several SNPs in DUSP12 and ATF6, located in chromosome 1q21-q23, were associated with type 2 diabetes.MethodsWe selected 19 single nucleotide polymorphisms (SNPs) that could tag 98% of the SNPs with minor allele frequencies over 0.1 within DUSP12-ATF6 region. These SNPs were genotyped in a total of 3,700 Chinese Han subjects comprising 1,892 type 2 diabetes patients and 1,808 controls with normal glucose regulation.ResultsNone of the SNPs and haplotypes showed significant association to type 2 diabetes in our samples. No association between the SNPs and quantitative traits was observed either.ConclusionsOur data suggests common SNPs within DUSP12-ATF6 locus may not play a major role in glucose metabolism in the Chinese.

【 授权许可】

Unknown   
© Hu et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.