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血管紧张素II 1型受体基因多态性对多囊卵巢综合征胰岛素抵抗的影响

Impact of angiotensin II type 1 receptor gene polymorphism on insulin resistance in polycystic ovary syndrome.

作者信息

El-Mesallamy H, El-Refaie T, El-Razek R A

机构信息

Biochemistry Department, Faculty of Pharmacy, Ain Shams University, Abassia, Cairo, Egypt.

出版信息

Exp Clin Endocrinol Diabetes. 2013 Apr;121(4):188-93. doi: 10.1055/s-0032-1333234. Epub 2013 Apr 5.

Abstract

Insulin resistance is allegedly a target pathophysiological mechanism in the pathogenesis of polycystic ovary syndrome. Moreover, this metabolic alteration is possibly genetically determined. In view of the recent evidence implicating genetic variants of the renin-angiotensin system as candidates in several metabolic disorders, we investigated the allele and genotype frequencies of the A1166 C polymorphism of the angiotensin II type 1 receptor in relation with various metabolic and biochemical parameters in affected females trying to asses its role in the pathogenesis of this syndrome. The study was conducted on 83 females of which 39 females served as the control group. The participants were matched for age, body mass index and degree of obesity. For all subjects biochemical parameters were assayed including soluble CD40 ligand together with fasting glucose and insulin which were used for calculation of insulin resistance indices, Genotyping performed using real time polymerase chain reaction revealed that the C allele frequency and the AC genotype were less frequently observed in patients compared to controls, however this difference was not statistically significant (p=0.146). Lack of the C allele was associated with adverse metabolic parameters including higher rate of insulin resistance as well as solubes CD40 ligand in the patients group. Results of the current study support a causative role for the A1166 C polymorphism of the angiotensin II type 1 gene polymorphism in the pathogenesis or phenotypic expression of polycystic ovary syndrome.

摘要

胰岛素抵抗被认为是多囊卵巢综合征发病机制中的一个关键病理生理机制。此外,这种代谢改变可能由基因决定。鉴于最近有证据表明肾素 - 血管紧张素系统的基因变异是几种代谢紊乱的候选因素,我们研究了1型血管紧张素II受体A1166C多态性的等位基因和基因型频率与受影响女性的各种代谢和生化参数之间的关系,试图评估其在该综合征发病机制中的作用。该研究对83名女性进行,其中39名女性作为对照组。参与者在年龄、体重指数和肥胖程度方面进行了匹配。对所有受试者进行了生化参数检测,包括可溶性CD40配体以及空腹血糖和胰岛素,后者用于计算胰岛素抵抗指数。使用实时聚合酶链反应进行基因分型显示,与对照组相比,患者中C等位基因频率和AC基因型的观察频率较低,然而这种差异无统计学意义(p = 0.146)。在患者组中,缺乏C等位基因与不良代谢参数相关,包括较高的胰岛素抵抗率以及可溶性CD40配体。本研究结果支持1型血管紧张素II基因A1166C多态性在多囊卵巢综合征发病机制或表型表达中的因果作用。

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