Role of the mitochondrial DNA 16184-16193 poly-C tract in type 2 diabetes

被引：53

作者：

Chinnery, PF ^{[1
]}

Elliott, HR

Patel, S

Lambert, C

Keers, SM

Durham, SE

McCarthy, MI

Hitman, GA

Hattersley, AT

Walker, M

机构：

[1] Univ Newcastle Upon Tyne, Mitochondrial Res Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

[2] Univ Newcastle Upon Tyne, Diabet Res Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

[3] Churchill Hosp, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX3 7LJ, England

[4] Barts & London Queen Marys Sch Med & Dent, Inst Cell & Mol Sci, Ctr Diabet & Metab Med, London, England

[5] Peninsula Med Sch, Exeter, Devon, England

来源：

LANCET | 2005年 / 366卷 / 9497期

基金：

英国惠康基金;

关键词：

D O I：

10.1016/S0140-6736(05)67492-2

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Recent evidence suggests that polymorphic genetic variation in the non-coding region of mitochondrial DNA (the 16184-16193 polycytosine [poly-C] tract) contributes to the cause of type 2 diabetes, but previous studies only just reached significance. We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184-16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1.16, 95% CI 0.94-1.44). Genetic variation of the 16184-16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes.

引用

收藏

页码：1650 / 1651

页数：2

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