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Serum gamma glutamyl transferase and magnesium as markers of oxidative stress in type2 diabetic patients

Author: 
Ritu Sharma and Mridula Mahajan
Subject Area: 
Health Sciences
Abstract: 

Background and Aims: Oxidative stress and adverse metabolic changes are key components of type2 diabetes mellitus. Gamma glutamyl transferase (GGT) enzyme maintains the GSH-cysteine homeostasis as well as detoxifies the toxic molecules thereby lower oxidative stress in the body. This enzyme is associated with albumin which is also a vital antioxidant molecule. Magnesium is required for the action of various glucose metabolizing enzymes and thus maintains glucose homeostasis as well as affects insulin secretion and sensitivity via modulation of oxidative stress. The purpose of the present study was to elucidate the role of serum GGT, magnesium and albumin in relation to hyperglycemia in type 2 diabetic patients. Method and Results: The study comprised of 50 diagnosed cases of type 2 diabetes mellitus and 30 age and sex matched healthy controls. Subjects were selected after applying appropriate inclusion and exclusion criterion. Written informed consent was obtained from all the subjects to draw their fasting blood samples under sterilized conditions. Diabetic patients were segregated into two Groups : Group 1 (fasting blood glucose levels 130-200mg/dl) and Group 2 (fasting blood glucose levels >200mg/dl). Serum GGT, magnesium, albumin and fasting blood glucose were estimated and data was statistically analyzed. Serum GGT activity was significantly high (p<0.05) and serum magnesium and albumin levels were significantly low (p<0.05) in type2 diabetic patients as compared to controls. A significant negative coefficient of correlation (p<0.05) was observed between Group 2 patients and their GGT activity. Conclusions: Increased serum GGT activity and low Mg and albumin levels are markers of high oxidative stress and metabolic disturbances in type 2diabetes. Body may try to compensate increased oxidative stress by preserving GSH by lowering of GGT activity in a state of increased hyperglycemia.

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