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QJM Advance Access published online on April 1, 2008

QJM, doi:10.1093/qjmed/hcn020
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© The Author 2008. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Assessment of oxidative stress and endothelial dysfunction in Asian Indians with type 2 diabetes mellitus with and without macroangiopathy

N. Singhania1, D. Puri1, S.V. Madhu2 and S.B. Sharma1

From the 1Department of Biochemistry and 2Department of Medicine, University College of Medical Sciences, Shahdara, Delhi, India

Address correspondence to Dr D. Puri, B-163, Yojana Vihar, Delhi-110092, India. email: dineshpuri21{at}yahoo.co.in

Received 12 September 2007 and in revised form 11 January 2008


   Abstract

Background: Enhanced oxidative stress coupled with increased expression of adhesion molecules (e.g. VCAM-1, ICAM-1) and decreased nitric oxide (NO) levels are implicated in development of atheromatous vascular lesion in diabetes. The present study addresses the correlation between oxidative stress, vascular cell adhesion molecules-1 (VCAM-1), NO end products and macroangiopathic complications in type 2 diabetes mellitus (DM).

Design and Methods: The study population consisted of three groups (i) diabetic patients with macroangiopathy (Group I); (ii) diabetic patients without macroangiopathy (Group II) and (iii) healthy controls (Group III) (n = 30, each group).

Results: Serum malondialdehyde(MDA) concentration was significantly higher in diabetic patients as compared to controls. Group I had significantly higher malondialdehyde level as compared to Group II (P < 0.05) (5.12 ± 1.83 µmol/l vs. 4.22 ± 1.03 µmol/l), suggesting higher oxidative stress in patients with macroangiopathy. Significant reduction in NO end products was observed in diabetic patients compared to controls. Levels of serum NO end products levels were further reduced in patients with macroangiopathy compared to those without macroangiopathy. Group I (971.67 ± 230.13 ng/ml) and Group II (823.55 ± 197.74 ng/ml) had significantly higher level of sVCAM-1 compared to healthy controls (541.14 ± 118.25 ng/ml) (P < 0.001). Also, patients with macroangiopathy had significantly higher levels of sVCAM-1 compared to those without macroangiopathy (P < 0.05). Multiple regression analysis indicated that post-prandial blood glucose, GSH and MDA were independent predictors of sVCAM-1 level (R = 0.690, P = 0.000).

Conclusion: It can be concluded from the present study that an enhanced oxidative stress coupled with endothelial dysfunction as indicated by reduced activity of NO pathway and enhanced expression of sVCAM-1 play an important intermediary role in the pathogenesis of macrovascular complications in type 2 DM.


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