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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Postprandial hypertriglyceridemia-induced endothelial dysfunction in healthy subjects is independent of lipid oxidation.
International Journal of Cardiology 2003 Februrary
BACKGROUND: To analyze the effects of postprandial hypertriglyceridemia with or without antioxidant supplementation-on endothelial function as related to lipid oxidation in healthy young subjects.
METHODS AND RESULTS: Ten healthy male subjects (mean age: 26 years) were examined three times in fasting state (10 hours) following a high-fat meal, a low-fat meal, or a high-fat meal with additional antioxidant vitamin E (800 IU), respectively. Serum triglycerides significantly increased 2 and 4 hours after eating the high-fat meal with or without additional vitamin E. Endothelium-dependent, flow-mediated brachial artery vasodilations (FMD; percentage change in diameter) changed from 13.3+/-1.1% to 6.6+/-1.1% (p<0.05), 7.1+/-0.6% (p<0.05), or 13.2+/-0.8% at 2, 4, or 6 hours after eating a high-fat meal. However, there were no changes of FMD observed following either a low-fat meal or a high-fat meal with additional vitamin E. The flow-dependent vasodilation inversely correlated to postprandial hypertriglyceridemia (r=-0.54, p<0.05). Serum malondialdehydes (MDA; lipid oxidation products) did not significantly change following ingestion of any of the 3 types of meal.
CONCLUSIONS: This study suggests that postprandial hypertriglyceridemia-induced endothelial dysfunction is not associated with lipid oxidation and that the protective effects of vitamin E on endothelial function may be due to some alternative, as of yet unknown, mechanism.
METHODS AND RESULTS: Ten healthy male subjects (mean age: 26 years) were examined three times in fasting state (10 hours) following a high-fat meal, a low-fat meal, or a high-fat meal with additional antioxidant vitamin E (800 IU), respectively. Serum triglycerides significantly increased 2 and 4 hours after eating the high-fat meal with or without additional vitamin E. Endothelium-dependent, flow-mediated brachial artery vasodilations (FMD; percentage change in diameter) changed from 13.3+/-1.1% to 6.6+/-1.1% (p<0.05), 7.1+/-0.6% (p<0.05), or 13.2+/-0.8% at 2, 4, or 6 hours after eating a high-fat meal. However, there were no changes of FMD observed following either a low-fat meal or a high-fat meal with additional vitamin E. The flow-dependent vasodilation inversely correlated to postprandial hypertriglyceridemia (r=-0.54, p<0.05). Serum malondialdehydes (MDA; lipid oxidation products) did not significantly change following ingestion of any of the 3 types of meal.
CONCLUSIONS: This study suggests that postprandial hypertriglyceridemia-induced endothelial dysfunction is not associated with lipid oxidation and that the protective effects of vitamin E on endothelial function may be due to some alternative, as of yet unknown, mechanism.
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