Objectives: To evaluate the association of glutathione S- transferase mu 1 (GST M1) and glutathione S- transferase theta 1 (GST T1) polymorphisms with the development of T1DM and disease-related risk factors. Materials and Methods: The study included 64 diabetic children with T1DM and 41 control subjects. They were subjected to: history taking anthropometric measurements and laboratory parameters included fasting glucose, serum creatinine, lipid profile, HbA1cand evaluation of GST T1 and M1 genetic polymorphisms using polymerase chain reaction (PCR).Results: There were significantly higher fasting glucose, glycosylated hemoglobin and cholesterol in the diabetic than the control group.GST T1 null genotype was more frequent in dia¬betic than
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GSTs are involved in the detoxification of ROS and in the synthesis of different inflammatory mediators. Both mechanisms can lead to pancreatic beta cell damage. So, it is hypothesized that GST polymorphisms may have a role in the pathogenesis of T1D. In our study, the associated risk of GST to T1D was investigated. Patients with T1D had a higher frequency of GST T1 null genotype than controls. This represented a significantly increased risk of T1D (4.2fold ).The combination of GST T1 null/ M1 wild genotype was significantly more frequent in diabetic patients than controls . This represented a significantly increased risk of T1D (3.2 fold ). Our findings are concordant with many previous studies on GST T1/M1 gene polymorphisms that reported an increased risk of T1D with null genotype[16,17,18,19]. This can be attributed to the fact that, carriers of GST null genotype have significantly lower antioxidant enzymatic activity [20]. However, Berkis et al.,2005 had reported that null genotype is protective gene regarding the risk of T1D[6].The difference from our study can be explained by several possible mechanisms; up-regulation of other antioxidant genes like superoxide dismutase gene that follows the depletion of GST activity., meaning while, these explanation possibilities needed to be confirmed in further research. Previous studies reported that GST T1 or M1 gene polymorphisms are regarded as a risk factor for the development of diabetes mellitus and chronic diabetic complications[13,21]. However, the results differ according to the authors, population, and the locality. Most of the data has been described in adult subjects with T2D[16,22].Very limited studies were conducted on GST polymorphisms and diabetes susceptibility in patients with T1D.Regarding GST T1
GSTs are involved in the detoxification of ROS and in the synthesis of different inflammatory mediators. Both mechanisms can lead to pancreatic beta cell damage. So, it is hypothesized that GST polymorphisms may have a role in the pathogenesis of T1D. In our study, the associated risk of GST to T1D was investigated. Patients with T1D had a higher frequency of GST T1 null genotype than controls. This represented a significantly increased risk of T1D (4.2fold ).The combination of GST T1 null/ M1 wild genotype was significantly more frequent in diabetic patients than controls . This represented a significantly increased risk of T1D (3.2 fold ). Our findings are concordant with many previous studies on GST T1/M1 gene polymorphisms that reported an increased risk of T1D with null genotype[16,17,18,19]. This can be attributed to the fact that, carriers of GST null genotype have significantly lower antioxidant enzymatic activity [20]. However, Berkis et al.,2005 had reported that null genotype is protective gene regarding the risk of T1D[6].The difference from our study can be explained by several possible mechanisms; up-regulation of other antioxidant genes like superoxide dismutase gene that follows the depletion of GST activity., meaning while, these explanation possibilities needed to be confirmed in further research. Previous studies reported that GST T1 or M1 gene polymorphisms are regarded as a risk factor for the development of diabetes mellitus and chronic diabetic complications[13,21]. However, the results differ according to the authors, population, and the locality. Most of the data has been described in adult subjects with T2D[16,22].Very limited studies were conducted on GST polymorphisms and diabetes susceptibility in patients with T1D.Regarding GST T1