Related Experiment Video
Updated: Aug 21, 2026

Bioluminescent Monitoring of Graft Survival in an Adoptive Transfer Model of Autoimmune Diabetes in Mice
Published on: November 18, 2022
Glutathione S-transferase T1 deletion is a risk factor for developing end-stage renal disease in diabetic patients
Yu Yang1, Min-Tsung Kao, Chia-Chu Chang
1Department of Molecular Medicine, China Medical University Hospital, 2, Yur Der Road, Taichung, Taiwan.
Abstract:
Reactive oxygen metabolites may contribute to the development of end-stage renal disease (ESRD) in diabetic and hypertensive patients. In this study, we used multiplex polymerase chain reaction (PCR) to analyze polymorphisms of two endogenous antioxidant genes, glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1), and to determine their role in the development of ESRD in diabetic and hypertensive patients. Our results showed that homozygous deletion of the GSTT1 gene is a risk factor for developing ESRD in diabetic patients (p=0.004, OR=2.18, 95% confidence interval (CI) =1.29-3.70), but not in hypertensive patients. No association between homozygous deletion of GSTM1 and the development of ESRD was found in either diabetic patients or hypertensive patients. These results indicate that genetic variations in enzymes involved in free radical metabolism are associated with the development of ESRD in diabetes mellitus (DM) patients, and may permit the targeting of preventive and early intervention strategies to high-risk individuals.
Related Concept Videos
Type I Diabetes I: Introduction
Diabetic Nephropathy
Type II Diabetes I: Introduction
Glucose Transporters
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Diabetes Mellitus: Overview and Type I Subtype
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Type I Diabetes II: Pathophysiology
