Chinnery P F, Elliott H R, Patel S, Lambert C, Keers S M, Durham S E, McCarthy M I, Hitman G A, Hattersley A T, Walker M
Mitochondrial Research Group, University of Newcastle upon Tyne, Newcastle upon Tyne, UK.
Lancet. 2005 Nov 5;366(9497):1650-1. doi: 10.1016/S0140-6736(05)67492-2.
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.
近期证据表明，线粒体DNA非编码区的多态性基因变异（16184 - 16193多聚胞嘧啶[poly - C]序列）与2型糖尿病的病因有关，但之前的研究仅勉强达到显著水平。我们旨在调查这种关联。我们将2型糖尿病患者（n = 992）与来自英国的两个独立对照组（n = 536，n = 1029）进行比较，发现16184 - 16193多聚 - C序列的频率没有差异。对欧洲1455例患者和3132例对照的研究进行的荟萃分析证实了这一发现（优势比1.16，95%可信区间0.94 - 1.44）。16184 - 16193多聚 - C序列的基因变异不太可能在2型糖尿病的病因中起主要作用。
Zotero 插件