Vitamin C Supplement Modulates Heat Shock Protein 72 Gene Expression in Skeletal Muscle of Rats with Type 2 Diabetes

Oxidative stress has been ascribed a role in the pathogenesis of diabetes and its complications and stress proteins have been shown to protect organisms in vitro and in vivo against oxidative stress. In this study we examined the HSP72 gene expression in skeletal muscle of type 2 diabetic rats induced by oral fructose administration (66% of total caloric intake) compared to control and the possibility to increase its level by oral administration of vitamin C (100mg/kg/day for 8 weeks). The amount of HSP72 m RNA in muscles of diabetic rats was lower than in control non-diabetic group (20.3±6.37 versus 40.52±7.49μg/g tissue) and its expression increased significantly by vitamin C administration (51.41±22.54μg/g tissue). There was an insignificant increase in muscle insulinstimulated glucose uptake after vitamin C administration in diabetic rats (2.59±0.66mg/g tissue versus 2±0.7mg/g tissue in diabetics not receiving vitamin C). The plasma glucose level following vitamin C administration in the diabetic group, showed a significant negative correlation with the expression of HSP72. The concentration of malondialdehyde (MDA) as a measure of lipid peroxidation increased significantly in diabetics (2.019±0.53μmol/g tissue) compared to control group (0.926±0.19μmol/g tissue) and administration of vitamin C in diabetic rats decreased the concentration of MDA insignificantly (1.55±0.47μmol/g tissue) compared to the diabetic group not receiving vitamin C. In conclusion, the finding of decreased levels of HSP72 expression and decreased insulinstimulated glucose uptake in skeletal muscle of type 2 diabetic rats raises the possibility that heat shock proteins may be involved in the pathogenesis of skeletal muscle insulin resistance in type 2 diabetics. Administration of vitamin C could be used in diabetics to increase heat shock protein HSP72 expression and to improve insulin resistance.