Department of Urology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
J Sex Med. 2012 Mar;9(3):837-43. doi: 10.1111/j.1743-6109.2011.02588.x. Epub 2012 Feb 3.
Accumulated evidences have outlined the potential relation between insulin resistance and endothelial dysfunction. The impaired ability of endothelium to synthesize or release nitric oxide may provide a common pathophysiological mechanism in the development of metabolic syndrome (MtS) and erectile dysfunction (ED).
The aim of this article was to investigate the genetic susceptibility of endothelial nitric oxide synthase (eNOS) G894T polymorphism underlying the development of both disorders.
A total of 590 subjects with a mean (standard deviation) age of 55.3 years (4.1) were enrolled during a free health screening. Complete clinical data and questionnaires were taken for all subjects. Multivariate logistic regression analysis was used to determine the independent predictors of MtS and ED. The eNOS G894T polymorphism was determined using a polymerase chain reaction-restriction fragment length polymorphism method.
The definition of MtS was according to the modified criteria developed by the Bureau of Health Promotion in Taiwan. Patients with ED were defined as those having a five-item International Index of Erectile Function (IIEF-5) <21.
Our results showed that the eNOS 894T allele carriers had significantly higher prevalence of MtS and ED (odds ratio [OR]=1.64, 95% confidence interval [CI]=1.05∼2.56, P=0.02 and OR=1.76, 95% CI=1.11∼2.80, P=0.01, respectively) after adjustment for each other and age. Also the T allele carriers had significantly lower IIEF-5 score and more MtS components than G allele carriers (P<0.01 and P<0.01, respectively), which were significantly associated with an increment of the T allele number (P<0.05).
The eNOS 894T allele carriers are at greater risk for both MtS and ED, suggesting that eNOS G894T gene polymorphism might play an implication as a common genetic susceptibility factor to develop both disorders.
越来越多的证据表明，胰岛素抵抗与内皮功能障碍之间存在潜在联系。内皮合成或释放一氧化氮的能力受损可能为代谢综合征（MtS）和勃起功能障碍（ED）的发展提供了共同的病理生理机制。
本文旨在研究内皮型一氧化氮合酶（eNOS）G894T 多态性在两种疾病发展中的遗传易感性。
在一次免费健康筛查中，共招募了 590 名平均（标准差）年龄为 55.3 岁（4.1）的受试者。对所有受试者进行了完整的临床数据和问卷调查。多变量 logistic 回归分析用于确定 MtS 和 ED 的独立预测因素。eNOS G894T 多态性采用聚合酶链反应-限制性片段长度多态性方法确定。
MtS 的定义依据台湾健康促进局制定的改良标准。ED 患者定义为国际勃起功能指数（IIEF-5）<21 的五项患者。
我们的结果表明，eNOS 894T 等位基因携带者的 MtS 和 ED 患病率显著升高（比值比[OR]=1.64，95%置信区间[CI]=1.05∼2.56，P=0.02 和 OR=1.76，95% CI=1.11∼2.80，P=0.01，分别），在相互调整和年龄后。此外，T 等位基因携带者的 IIEF-5 评分显著较低，MtS 成分也显著高于 G 等位基因携带者（P<0.01 和 P<0.01，分别），这与 T 等位基因数量的增加显著相关（P<0.05）。
eNOS 894T 等位基因携带者患 MtS 和 ED 的风险更高，表明 eNOS G894T 基因多态性可能作为一种共同的遗传易感性因素，导致两种疾病的发生。
