Introduction: Evidence has long existed regarding the relationship between oxidative stress and diabetes. The present study was conducted to assess the effect of atorvastatin on selected oxidative stress parameters in the form of reduced glutathione (GSH), lipid peroxidation byproduct malondialdehyde (MDA) levels, glutathione –S- transferase (GST) activity and catalase (CAT) activity) and its effect on lipid profile (total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) in dyslipidaemic type 2 diabetic patients . Materials and Methods: Fifty nine dyslipidaemic type 2 diabetic patients were included in this study. Full history was taken and general examination of patients was performed. Patients studied were taking glibenclamide (an oral hypoglycaemic drug) during the study as a treatment for their disease. These patients were followed up for 60 days and divided randomly into 2 groups. Group I (n = 31): no drug was given and served as dyslipidaemic diabetic control. Group II (n = 28): received atorvastatin tablets 20 mg once daily at night. Of the 59 Fifty patients, 46 completed the study while 13 patients withdrew. This is due to non compliance of the patients. Blood samples were drawn from the patients at the beginning and after 60 days of follow up between 8:30 & 10:30 am after at least 12-14 hours fast. Fasting blood glucose, lipid profile, selected oxidative stress parameters (GSH, MDA levels, GST and CAT activities) were measured. Renal and hepatic functions were also assessed. Results: This study revealed that: atorvastatin treatment increased serum GSH; reduced MDA levels significantly while did not significantly affect CAT and GST activity. In atorvastatin treatment, TC, TG, LDL and VLDL decreased significantly while HDL increased significantly. Conclusion: There was insignificant correlations between atorvastatin induced changes in the oxidation markers and the observed changes of the lipid profile.
Low-Dose Acrolein, an Endogenous and Exogenous Toxic Molecule, Inhibits Glucose Transport via an Inhibition of Akt-Regulated GLUT4 Signaling in Skeletal Muscle Cells
