Among the primary human classes of glutathione S-transferase (GST) genes, GSTM1 and GSTT1 genes exhibit a deletion polymorphism that leads to a lack of active isoforms when in homozygous state(the null genotype). Persons with homozygous deletions of either GSTM1 or GSTT1 locus have no functional enzymatic activity of GST and this in turn exacerbate the damage caused by ROS and RNS to pancreatic β-cells. This causes reduced insulin production and, therefore type 2 diabetes. Therefore, GST polymorphic genes (GSTM1-null and GSTT1-null) could be used as a biological marker to determine the diabetic risk of individual.
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