Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress

Bae, Jang–Ho; Bassenge, E.; Kim, Kwon-Bae; Kim, Yoon-Nyun; Kim, Kee‐Sik; Lee, Hee-Ja; Moon, Kyo-Cheol; Lee, Moo‐Sik; Park, Keun-Yong; Schwemmer, Michael

doi:10.1016/s0021-9150(00)00601-8

Cited by 319 publications

(289 citation statements)

References 31 publications

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“…Damage to cellular structures such as proteins, carbohydrates, nucleic acids and lipids can result from oxidative processes during this time. Increased postprandial oxidation is a major contributor to atherosclerosis and endothelium dysfunction (Bae et al, 2001). Today, many in vitro and ex vivo assays exist for the assessment of oxidative stress and have been described in detail elsewhere (Moore and Roberts, 1998).…”

Section: Tracers With Stable Isotopesmentioning

confidence: 99%

Methodology for studying postprandial lipid metabolism

2007

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Background: Postprandial lipid metabolism in humans has deserved much attention during the last two decades. Although fasting lipid and lipoprotein parameters reflect body homeostasis to some extent, the transient lipid and lipoprotein accumulation that occurs in the circulation after a fat-containing meal highlights the individual capacity to handle an acute fat input. An exacerbated postprandial accumulation of triglyceride-rich lipoproteins in the circulation has been associated with an increased cardiovascular risk. Methods: The important number of studies published in this field raises the question of the methodology used for such postprandial studies, as reviewed. Results: Based on our experiences, the present review reports and discuss the numerous methodological issues involved to serve as a basis for further works. These aspects include aims of the postprandial tests, size and nutrient composition of the test meals and background diets, pre-test conditions, characteristics of subjects involved, timing of sampling, suitable markers of postprandial lipid metabolism and calculations. Conclusion: In conclusion, we stress the need for standardization of postprandial tests.

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Section: Tracers With Stable Isotopesmentioning

confidence: 99%

Methodology for studying postprandial lipid metabolism

2007

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“…6,7 Similarly, a negative influence of postprandial hypertriglyceridemia on endothelial function has been reported in both normal and diabetic subjects. 8,9 It has been suggested that hyperglycemia 6 -7 and hypertriglyceridemia 8 -9 induce an endothelial dysfunction through the production of an oxidative stress. The process may involve the overgeneration of superoxide anion (O 2 Ϫ ), which in turn inactivates nitric oxide (NO).…”

Section: P Atients With Diabetes Have An Increased Risk Of Cardiovascmentioning

confidence: 99%

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

et al. 2002

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Background-Postprandial hypertriglyceridemia and hyperglycemia are considered risk factors for cardiovascular disease.Evidence suggests that postprandial hypertriglyceridemia and hyperglycemia induce endothelial dysfunction through oxidative stress; however, the distinct role of these two factors is a matter of debate. Methods and Results-Thirty type 2 diabetic patients and 20 normal subjects ate 3 different meals: a high-fat meal; 75 g glucose alone; and high-fat meal plus glucose. Glycemia, triglyceridemia, nitrotyrosine, and endothelial function were assayed during the tests. Subsequently, diabetics took 40 mg/d simvastatin or placebo for 12 weeks. The 3 tests were performed again at baseline, between 3 to 6 days after the start, and at the end of each study. High-fat load and glucose alone produced a decrease of endothelial function and an increase of nitrotyrosine in normal and diabetic subjects. These effects were more pronounced when high fat and glucose were combined. Short-term simvastatin treatment had no effect on lipid parameters but reduced the effect on endothelial function and nitrotyrosine observed during each different test. Long-term simvastatin treatment was accompanied by a lower increase in postprandial triglycerides, which was followed by smaller variations of endothelial function and nitrotyrosine during the tests. Conclusions-This study shows an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function, suggesting oxidative stress as common mediator of such effect. Simvastatin shows a beneficial effect on oxidative stress and endothelial dysfunction, which may be ascribed to a direct effect as well as the lipid-lowering action of the drug.

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“…Although triglyceride levels are consistently measured in fasting blood specimens, accumulating evidence indicates that postprandial triglycerides further increase oxidative stress (8) and are an under-recognized contributing factor to endothelial dysfunction, atherosclerosis, and cardiovascular events (9).…”

mentioning

confidence: 99%

Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome

et al. 2007

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OBJECTIVE -The aim of this study was to determine the effects of fenofibrate (160 mg/day) on fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediators in subjects with hypertriglyceridemia and the metabolic syndrome.RESEARCH DESIGN AND METHODS -Fifty-nine subjects with fasting hypertriglyceridemia (Ն1.7 and Ͻ6.9 mmol/l) and two or more of the Adult Treatment Panel III criteria for the metabolic syndrome were randomly assigned to fenofibrate (160 mg/day) or placebo in a double-blind, controlled clinical trial.RESULTS -Fenofibrate treatment lowered fasting triglycerides (Ϫ46.1%, P Ͻ 0.0001) and postprandial (area under the curve) triglycerides (Ϫ45.4%, P Ͻ 0.0001) due to significant reductions in postprandial levels of large (Ϫ40.8%, P Ͻ 0.0001) and medium (Ϫ49.5%, P Ͻ 0.0001) VLDL particles. The number of fasting total LDL particles was reduced in fenofibratetreated subjects (Ϫ19.0%, P ϭ 0.0033) primarily due to reductions in small LDL particles (Ϫ40.3%, P Ͻ 0.0001); these treatment differences persisted postprandially. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared with placebo-administered subjects (Ϫ15.3%, P ϭ 0.0013, and 31.0%, P Ͻ 0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble vascular cell adhesion molecule-1 (VCAM-1) (Ϫ10.9%, P ϭ 0.0005, and Ϫ12.0%, P ϭ 0.0001, respectively) as well as fasting and postprandial soluble intercellular adhesion molecule-1 (ICAM-1) (Ϫ14.8%, P Ͻ 0.0001, and Ϫ15.3%, P Ͻ 0.0001, respectively). Reductions in VCAM-1 and ICAM-1 were correlated with reductions in fasting and postprandial large VLDL particles (P Ͻ 0.0001) as well as postprandial oxidized fatty acids (P Ͻ 0.0005).CONCLUSIONS -Triglyceride-lowering therapy with fenofibrate reduced fasting and postprandial free fatty acid oxidation and inflammatory responses, and these antiatherosclerotic effects were most highly correlated with reductions in large VLDL particles. Diabetes Care 30:1945-1951, 2007T he metabolic syndrome represents an agglomeration of interrelated risk factors that include abnormally high fasting triglyceride levels (1,2). In a recent analysis, hypertriglyceridemia (Ն1.7 mmol/l) represented the component of the metabolic syndrome most strongly associated with a history of myocardial infarction and stroke (3). Furthermore, elevated fasting triglyceride levels (Ն1.4 mmol/l) and an enlarged waist circumference (Ͼ89 cm) were the two characteristics of the metabolic syndrome that were associated with the greatest increased risk for all-cause mortality and cardiovascular deaths among postmenopausal women (4).Hypertriglyceridemia signifies the presence of increased plasma triglycerideremnant lipoproteins, and the concentrations of remnant-like lipoproteins are further enhanced postprandially among hypertriglyceridemic subjects (5). Remnant-like proteins have been shown to increase intracellular oxidant concentrations and lipid peroxide levels in culture media and to activate nuclear factor-B ...

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Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress

Cited by 319 publications

References 31 publications

Methodology for studying postprandial lipid metabolism

Methodology for studying postprandial lipid metabolism

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome

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