摘要
目的探讨2型糖尿病(T2DM)患者内皮一氧化氮合酶(eNOS)基因5′-侧翼区T-786→C突变与T2DM患者内皮依赖性血管舒张功能(EDD)关系。方法选择无血管并发症的男性T2DM患者162例。采用PCR/ASO探针杂交技术检测eNOS基因5′-侧翼区T-786→C突变。采用高分辨超声检测肱动脉血流介导的EDD。结果T/C或C/C组EDD为3·73%±0·50%,明显低于T/T组(4·15%±0·49%)(P<0·01)。多元逐步分析结果显示,在所有T2DM患者中,EDD与C等位基因呈负相关(P=0·001)。在吸烟者中,T/C或C/C组EDD明显低于T/T组(P<0·05),在非吸烟者中则不然。多元逐步分析结果显示,在吸烟者中,C等位基因是EDD下降的独立危险因子(P<0·01),在非吸烟者中则不然。结论eNOS基因5′-侧翼区T-786→C突变是T2DM患者内皮功能异常的遗传危险因子,尤其是吸烟的T2DM患者。
Objective To assess whether the T^-786→C mutation of endothelial nitric oxide synthase （eNOS） gene is associated with endothelial dysfunction in type 2 diabetes. Methods A total of 162 type 2 diabetic men without angiopathy were studied. PCR/alleles-specific oligonucleotide （ASO） probes were used to analyse the T^-786→C mutation of eNOS gene, and high resolution ultrasound was used to measure endothelium-dependent arterial dilation （EDD）. Results The EDD among subjects with T/C or C/C was 3.73 %±0.50 %, which was significantly lower than that in subjects with T/T （4. 15%±0.49%） （P〈0.01）. On stepwise multiple regression analysis, EDD was negatively correlated with C allele in all patients （P： 0. 001）. EDD in smokers with T/C or C/C was significantly lower than that in smokers with T/T （P〈0.05） but not in nonsmokers. The stepwise multiple regression analysis revealed that the presence of C allele was an independent determinant for reduced EDD in smokers （P〈0. 001）, but not in nonsmokers. Conclusions The C allele of T^-786→C mutation of eNOS gene is a genetic risk factor for endothelial dysfunction in type 2 diabetic patients, especially in smokers.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2006年第5期346-348,共3页
Chinese Journal of Diabetes
基金
湖北省卫生厅科研课题资助项目(JX2B44)
关键词
糖尿病
2型
内皮
血管
一氧化氮合酶
多态性
Diabetes mellitus, type 2
Endothelium, vascular
Nitric oxide synthase
Polymorphism
