Abstract
BACKGROUND: Oxidative stress has become a real entity in etiopathogenesis of Type 2 diabetes mellitus (DM). It may result from steady flux of free radicals and lipid peroxides in vivo. Malondialdehyde (MDA) is a stable end product of lipid peroxidation. Accumulative evidences suggest that hyperglycemia in Type 2 DM can produce major changes in nitric oxide (NO) production as well as in its action. Alteration in metabolism of trace elements is also observed in DM. OBJECTIVE: To evaluate oxidative stress, status of NO, and trace elements zinc (Zn) and magnesium (Mg) in type 2 DM and to correlate these parameters with disease process. MATERIALS AND METHODS: Ninety-two cases with diabetes were included in the study, out of which 51 were type 2 DM without any complication and 41 were type 2 DM with complications. Fifty-one nondiabetic healthy controls from hospital staff were selected for the study. Blood samples were collected after an overnight fast for estimation of fasting plasma glucose, postprandial glucose, glycated hemoglobin (HbA1c), lipid profile, trace element status, MDA, and NO. RESULTS: Study revealed a rise in MDA levels in both uncomplicated and complicated cases with diabetes (2.47 ± 0.53, 3.98 ± 0.42 nmol/ml, respectively) as compared to controls (1.43 ± 0.23 nmol/ml), which was statistically significant (P < 0.05). The mean levels of NO, Zn, and Mg were significantly lower in both the diabetic groups than the control group (P < 0.05). MDA showed a significant positive correlation with plasma glucose, lipid profile parameters (except high-density lipoprotein cholesterol), and significant negative correlation with Zn (r = -0.44, P < 0.05) and Mg (r = -0.31, P < 0.05). NO levels were correlated significantly with plasma glucose, dyslipidemia, and HbA1c (P < 0.05). The effects of glycemic status on trace element concentrations were evident from a significant negative correlation between Zn and Mg with fasting plasma glucose and HbA1c. CONCLUSION: Findings of the present study may establish the role of hyperglycemia, oxidative stress, impaired NO, and trace elements in pathogenesis and long-term vascular complications of type 2 DM.