El-Sawaf, A., Fayed, H. (2007). Effect of Vitamin E on Blood Glucose, Insulin, Lipid Peroxides, and Antioxidant System of Streptozotocin-Induced Diabetes in Rats. Journal of High Institute of Public Health, 37(1), 19-31. doi: 10.21608/jhiph.2007.22012
Amel El-Sawaf; Hassan Fayed. "Effect of Vitamin E on Blood Glucose, Insulin, Lipid Peroxides, and Antioxidant System of Streptozotocin-Induced Diabetes in Rats". Journal of High Institute of Public Health, 37, 1, 2007, 19-31. doi: 10.21608/jhiph.2007.22012
El-Sawaf, A., Fayed, H. (2007). 'Effect of Vitamin E on Blood Glucose, Insulin, Lipid Peroxides, and Antioxidant System of Streptozotocin-Induced Diabetes in Rats', Journal of High Institute of Public Health, 37(1), pp. 19-31. doi: 10.21608/jhiph.2007.22012
El-Sawaf, A., Fayed, H. Effect of Vitamin E on Blood Glucose, Insulin, Lipid Peroxides, and Antioxidant System of Streptozotocin-Induced Diabetes in Rats. Journal of High Institute of Public Health, 2007; 37(1): 19-31. doi: 10.21608/jhiph.2007.22012
Effect of Vitamin E on Blood Glucose, Insulin, Lipid Peroxides, and Antioxidant System of Streptozotocin-Induced Diabetes in Rats
Departments of Physiology and Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt
Abstract
Background: There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress which further exacerbates the development and progression of diabetes and its complications. There are multiple sources of oxidative stress in diabetes including non-enzymatic, enzymatic, and mitochondrial pathways. Vitamin E is a fat-soluble vitamin that prevents lipid peroxidation. Objective: the present study was carried out to test the effect of vitamin E on blood glucose, insulin, and lipid peroxides in blood and liver tissue of rats in relation to oxidative damage associated with diabetes induced by streptozotocin (STZ). Methods: 24 male albino rats were randomly assigned to control (group I), streptozotocin (STZ)-induced diabetic rats (group II), the third group (vitamin E group) were STZ-induced diabetic rats fed 400 mg of vitamin E/kg diet. After 4 weeks of the induction of diabetes, rats were sacrificed and the following determinations were done on the blood, serum or plasma. Blood glucose, serum insulin, lipid peroxide concentration in plasma as malonyldialdehyde (MDA) level in nmol/g protein, the amount of thiobarbituricp acid reactive materials in plasma (TBARM), serum antioxidant capacity (assayed by measuring the total peroxy radical trapping capacity (TRAP) of serum, and serum superoxide dismutase, enzyme activity (SOD). In the liver, the following parameters were determined: liver MDA, SOD and Glutathione peroxidase (GSH-Px) enzyme activaties, and Glutathione (GSH) concentration. Results: Hyperglycemia, hypoinsulinemia were regarded in group II which were ameliorated by vitamin E administration. Oxidant stress was found in diabetic rats group II manifested by increase concentration of MDA-plasma and liver, increase TBARM concentration, and TRAP-plasma and serum respectively. Also increased serum SOD, liver SOD, and GSH-Px enzyme activities in these diabetic rats. Administration of vitamin E in the diet decreased the oxidant stress parameters (MDA, TBARM, and TRAP), increased the antioxidant defense parameter (increased GSH concentration in liver), and decreased the oxidant stress as manifested by the decrease in serum SOD enzyme activity; liver SOD; and GSH-Px enzyme activities. Conclusion: Vitamin E was found to be excellent for strengthening the antioxidant defense system in STZ-diabetic rats and it may therefore have a therapeutic role in combating the damaging effect of ROS in diabetes and preventing its complications.
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