title: Supplementation of a γ-tocopherol-rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by postprandial hyperglycemia.
abstract: Postprandial hyperglycemia induces oxidative stress responses, impairs vascular endothelial function (VEF) and increases the risk of cardiovascular disease. We hypothesized that the antioxidant and anti-inflammatory activities of a γ-tocopherol-rich mixture of tocopherols (γ-TmT) would protect against vascular dysfunction that is otherwise caused by postprandial hyperglycemia by decreasing oxidative stress and proinflammatory responses, and improving nitric oxide (NO•) homeostasis. In a randomized, crossover study, healthy men (n=15; 21.8 ± 0.8 years) completed a fasting oral glucose challenge (75 g) with or without prior supplementation of γ-TmT (5 days). Brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine and asymmetric dimethylarginine (ADMA) were measured at regular intervals during a 3-h postprandial period. Supplementation of γ-TmT increased (P<.05) plasma γ-T by threefold and γ-carboxyethyl-hydroxychroman by more than ninefold without affecting α-T, glucose, arginine or ADMA. Baseline FMD, MDA, arginine and ADMA were unaffected by γ-TmT (P>.05). Postprandial FMD decreased 30%-44% (P<.05) following glucose ingestion, but was maintained with γ-TmT. Supplementation of γ-TmT also attenuated postprandial increases in MDA that occurred following glucose ingestion. Plasma arginine decreased (P<.05) in both trials to a similar extent regardless of γ-TmT supplementation. However, the ratio of ADMA/arginine increased time-dependently in both trials (P<.05), but to a lesser extent following γ-TmT supplementation (P<.05). Inflammatory proteins were unaffected by glucose ingestion or γ-TmT. Collectively, these findings support that short-term supplementation of γ-TmT maintains VEF during postprandial hyperglycemia possibly by attenuating lipid peroxidation and disruptions in NO• homeostasis, independent of inflammation.
authors: Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269-4010, USA.
authors: Eunice
authors: E
authors: Mah
authors: Sang K
authors: SK
authors: Noh
authors: Kevin D
authors: KD
authors: Ballard
authors: Hea Jin
authors: HJ
authors: Park
authors: Jeff S
authors: JS
authors: Volek
authors: Richard S
authors: RS
authors: Bruno
mesh_terms: D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000032:analysis / Q000378:metabolism; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D001205:Ascorbic Acid / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D001916:Brachial Artery / Q000187:drug effects / Q000503:physiopathology; D019587:Dietary Supplements; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology* / Q000517:prevention & control*; D007328:Insulin / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D024505:Tocopherols / Q000737:chemistry / Q000627:therapeutic use; D014527:Uric Acid / Q000097:blood; D055815:Young Adult; D024504:gamma-Tocopherol / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D007328:Insulin; D014527:Uric Acid; D009569:Nitric Oxide; D008315:Malondialdehyde; C018524:N,N-dimethylarginine; D024504:gamma-Tocopherol; D001120:Arginine; D001205:Ascorbic Acid; D024505:Tocopherols