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γ‐Tocopherol supplementation improves postprandial vascular endothelial function in lean and obese men by decreasing oxidative and nitrative stress
Author(s) -
Mah Eunice,
Ballard Kevin D,
Kawiecki Diana M,
Volek Jeff S,
Bruno Richard S
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.535.6
Subject(s) - postprandial , medicine , oxidative stress , malondialdehyde , endocrinology , endothelial dysfunction , brachial artery , inflammation , insulin , blood pressure
Hyperglycemia induces oxidative stress and inflammation that impairs vascular endothelial function (VEF). We hypothesized that γ‐tocopherol (γ‐T) supplementation would improve hyperglycemia‐mediated decreases in VEF by reducing oxidative stress and inflammatory responses. A randomized, crossover study was conducted in lean and obese men (n=8/group) who followed their usual diet or were also provided γ‐T‐rich capsules (500 mg/d, 5 d) prior to an oral glucose challenge. Brachial artery flow‐mediated dilation (FMD) and markers of oxidative/nitrative stress and inflammation were measured throughout the 3 h postprandial period. Supplementation increased plasma γ‐T by 170% in all men without affecting α‐T. Baseline HOMA was greater in obese men and correlated to FMD, but was unchanged by γ‐T. Postprandial hyperglycemia decreased FMD (p<0.05) in both groups. Postprandial FMD area under the curve (AUC) increased in both groups following γ‐T supplementation consistent with greater baseline FMD. Baseline nitro‐γ‐T and total cysteine and postprandial malondialdehyde AUC were lower in all men following γ‐T whereas myeloperoxidase and C‐reactive protein were unchanged. Thus, short‐term γ‐T supplementation likely improves VEF by decreasing oxidative and nitrative damage, but without affecting insulin resistance or inflammatory responses. Support provided by International Life Sciences Institute to RSB. Grant Funding Source : International Life Sciences Institute