Supplementation of a γ-tocopherol-rich mixture of tocopherols in healthy men protects against vascular endothelial dysfunction induced by postprandial hyperglycemia

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 gamma-tocopherol-rich mixture of tocopherols (gamma-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 center dot) 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 gamma-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 gamma-TmT increased (P<.05) plasma gamma-T by threefold and gamma-carboxyethyl-hydroxychroman by more than ninefold without affecting alpha-T, glucose, arginine or ADMA. Baseline FMD, MDA, arginine and ADMA were unaffected by gamma-TmT (P>.05). Postprandial FMD decreased 30%-44% (P<.05) following glucose ingestion, but was maintained with gamma-TmT. Supplementation of gamma-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 gamma-TmT supplementation. However, the ratio of ADMA/arginine increased time-dependently in both trials (P<.05), but to a lesser extent following gamma-TmT supplementation (P<.05). Inflammatory proteins were unaffected by glucose ingestion or gamma-TmT. Collectively, these findings support that short-term supplementation of gamma-TmT maintains VEF during postprandial hyperglycemia possibly by attenuating lipid peroxidation and disruptions in NO center dot homeostasis, independent of inflammation. Published by Elsevier Inc.