Dadbinpour Alamdar, Sheikhha Mohammad Hasan, Darbouy Mojtaba, Afkhami-Ardekani Mohammad
Yazd Diabetes Research Center, Shahid Sadoughi University of Medical Sciences, Jomhori Boulevard, Yazd, Iran.
J Diabetes Metab Disord. 2013 Dec 19;12(1):48. doi: 10.1186/2251-6581-12-48.
Diabetes is one of the multifactorial disorders with genetics and environmental factors playing important role in its cause. In diabetes, the defects in cellular metabolism results in increasing free radicals. These radicals react with other vital cellular molecules which are responsible in diabetes side effects. Human glutathione S-transferases (GST) are a family of enzymes that catalyses conjugation of electrophilic substances with glutathione. In this research the deletion of two of the most important genes of this family; GSTT1 and GSTM1 genes was investigated as the risk factor for diabetes mellitus type II and one of its most important complications; retinopathy.
In this study deletion of GSTT1 and GSTM1 genes in 57 diabetics' patients with retinopathy and 58 diabetic peoples without retinopathy was examined. DNA was extracted from peripheral blood and then multiplex PCR was performed following agarose gel electrophoresis to detect GSTT1 and GSTM1 null genotypes. Data were analyzed with SPSS v16 software.
The results indicated that there was significant relationship between GSTM1 null genotype with retinopathy side effect of diabetes type 2. While there was no significant relationship between GSTT1 null genotypes with retinopathy in diabetes type 2.
Significant correlation between GSTM1 null genotype and retinopathy in this and other studies could indicate this fact that impair cellular metabolism result in increase free radicals and oxidative pressure. Therefore, GST null genotypes may result in decrease antioxidant capacity which causes side effects of diabetes. Considering the performance of different classes of GST null genotypes additional studies are required to confirm this study.
糖尿病是一种多因素疾病,遗传和环境因素在其病因中起着重要作用。在糖尿病中,细胞代谢缺陷导致自由基增加。这些自由基与导致糖尿病副作用的其他重要细胞分子发生反应。人类谷胱甘肽S-转移酶(GST)是一类催化亲电物质与谷胱甘肽结合的酶。在本研究中,对该家族两个最重要基因GSTT1和GSTM1基因的缺失作为2型糖尿病及其最重要并发症之一视网膜病变的危险因素进行了研究。
在本研究中,检测了57例患有视网膜病变的糖尿病患者和58例无视网膜病变的糖尿病患者中GSTT1和GSTM1基因的缺失情况。从外周血中提取DNA,然后在琼脂糖凝胶电泳后进行多重PCR,以检测GSTT1和GSTM1无效基因型。数据用SPSS v16软件进行分析。
结果表明,GSTM1无效基因型与2型糖尿病视网膜病变副作用之间存在显著关系。而GSTT1无效基因型与2型糖尿病视网膜病变之间无显著关系。
本研究及其他研究中GSTM1无效基因型与视网膜病变之间的显著相关性可能表明,细胞代谢受损导致自由基增加和氧化压力增加。因此,GST无效基因型可能导致抗氧化能力下降,从而引起糖尿病的副作用。考虑到不同类型GST无效基因型的表现,需要进一步研究来证实本研究。