Postprandial hypertriglyceridemia-induced endothelial dysfunction in healthy subjects is independent of lipid oxidation

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 fastin...

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Published in:International journal of cardiology Vol. 87; no. 2; pp. 259 - 267
Main Authors: Bae, Jang-Ho, Schwemmer, Michael, Lee, In-Kyu, Lee, Hee-Ja, Park, Ki-Rack, Kim, Ki-Young, Bassenge, Eberhard
Format: Journal Article
Language:English
Published: Shannon Elsevier Ireland Ltd 01-02-2003
Elsevier Science
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Summary: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.
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ISSN:0167-5273
1874-1754
DOI:10.1016/S0167-5273(02)00347-9