Effect of oral vitamin E (α-tocopherol) supplementation on vascular endothelial function in Type 2 diabetes mellitus

Summary Aims Vascular endothelial dysfunction, an early marker of atherosclerosis, has been demonstrated in Type 2 diabetes mellitus (DM). Vitamin E preserves endothelial function in animal models of diabetes and reduces cardiovascular risk. We examined endothelial function and the effect of vitamin...

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Published inDiabetic medicine Vol. 16; no. 4; pp. 304 - 311
Main Authors Gazis, A., White, D. J., Page, S. R., Cockcroft, J. R.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.04.1999
Blackwell
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Summary:Summary Aims Vascular endothelial dysfunction, an early marker of atherosclerosis, has been demonstrated in Type 2 diabetes mellitus (DM). Vitamin E preserves endothelial function in animal models of diabetes and reduces cardiovascular risk. We examined endothelial function and the effect of vitamin E supplements in uncomplicated Type 2 DM. Methods Forty‐eight subjects with Type 2 DM and 21 controls had endothelial function assessed using forearm venous occlusion plethysmography with endothelium‐independent (sodium nitroprusside) and dependent (acetylcholine, bradykinin) vasodilators. Those with diabetes received 1600 iu daily oral α‐tocopherol or placebo, double‐blind for 8 weeks, and had endothelial function reassessed. Results The diabetic group had higher HbA1c (6.9 ± 1.4 vs 4.8 ± 0.6%; P < 0.01) and systolic (145 ± 15 vs 130 ± 16 mmHg; P < 0.01) but not diastolic blood pressure (79 ± 8 vs 76 ± 9 mmHg; P = 0.15). There was blunted vasodilation to acetylcholine (15 μg/min; P < 0.01) in subjects with diabetes. Vasodilation to sodium nitroprusside and bradykinin was similar (all P > 0.1). α‐tocopherol did not affect vasodilation to nitroprusside (P > 0.1), acetylcholine (P > 0.1) or bradykinin (P > 0.1). Conclusions There may be receptor‐specific endothelial dysfunction in subjects with uncomplicated Type 2 DM. This is not improved by treatment with α‐tocopherol. Diabet. Med. 16, 304–311 (1999)
Bibliography:istex:2491178A3980CBA2560EA7310E005D95BB996616
ArticleID:DME049
ark:/67375/WNG-NHNW5CCF-D
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
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ISSN:0742-3071
1464-5491
DOI:10.1046/j.1464-5491.1999.00049.x