Effects of oxidative stress on endothelial function after a high-fat meal

2004 ◽  
Vol 106 (3) ◽  
pp. 315-319 ◽  
Author(s):  
Wei-Chuan TSAI ◽  
Yi-Heng LI ◽  
Chih-Chan LIN ◽  
Ting-Hsing CHAO ◽  
Jyh-Hong CHEN

Postprandial lipaemia is known to cause endothelial dysfunction, but its underlying mechanism is still under debate. The present study was undertaken to investigate the effects of postprandial lipaemia on endothelial dysfunction and oxidative stress. We measured plasma glutathione peroxidase (GSH-Px), an antioxidant enzyme, and the urinary excretion of 8-epi-prostaglandin F2α (8-PGF2α), a free radical-catalysed product from the oxidative modification of arachidonic acid, in 16 healthy subjects (mean age, 30±5 years) without major coronary risk factors. Plasma high-sensitive C-reactive protein, soluble intercellular cell-adhesion molecule-1 and vascular cell-adhesion molecule-1 were also measured. High-resolution ultrasound was used to assess the flow-mediated vasodilatation (FMD) of the brachial artery. Blood and urine samples were collected before and 2, 4 and 6 h after a standard high-fat meal (3677 J, containing 50 g of fat). Serum triacylglycerol (triglyceride) increased and FMD decreased significantly after a high-fat meal. Plasma GSH-Px significantly decreased from 27.2±12.3 µg/ml to 25.7±11.8 µg/ml (P=0.022) 2 h after the meal, and urinary excretion of 8-PGF2α significantly increased from 1286±1401 pg/mg of creatinine to 2197±1343 pg/mg of creatinine (P=0.014) at 4 h after the meal. However, there were no significant changes in the levels of high-sensitive C-reactive protein and adhesion molecules after a high-fat meal. In conclusion, endothelial dysfunction was observed after consuming a high-fat meal and is associated with augmented oxidative stress manifested by the depletion of serum antioxidant enzymes and increased excretion of oxidative modification products.

2017 ◽  
Vol 118 (8) ◽  
pp. 607-615 ◽  
Author(s):  
Thaís da S. Ferreira ◽  
Vanessa P. Antunes ◽  
Priscila M. Leal ◽  
Antonio F. Sanjuliani ◽  
Márcia R. S. T. Klein

AbstractNon-fasting hypertriacylglycerolaemia is a risk factor for CVD and the amount of fat in a meal seems to be the main factor influencing postprandial lipaemia. Although several studies suggest that Ca can increase faecal fat excretion, it is not known whether Ca can decrease postprandial TAG. This study aimed to evaluate the influence of dietary Ca (DC) and supplemental Ca (SC) on lipaemia, glucose metabolism, C-reactive protein (CRP) and adiponectin during postprandial period in obese women challenged with a high-fat meal. In this cross-over controlled trial, sixteen obese women aged 20–50 years were randomly assigned to receive three test meals (approximately 2900 kJ; 48 % fat): high DC (547 mg DC), high SC (HSCM; 500 mg SC-calcium carbonate) and low Ca (42 mg DC). Blood samples were collected in the fasting period and at minutes 120 and 240 after meals to evaluate total cholesterol and fractions, TAG, glucose, insulin, high-sensitivity CRP and adiponectin. Serum levels of TAG and insulin increased significantly after all test meals. Only after HSCM total cholesterol did not present a significant increase and LDL-cholesterol had a significant decrease. Postprandial glucose, HDL-cholesterol, CRP and adiponectin did not present significant changes after the three test meals. The comparative analysis of the effects of the three test meals on serum lipids, glucose, insulin, CRP and adiponectin revealed no significant meal-by-time interaction. These results suggest that in obese women challenged with a high-fat meal DC and SC do not interfere with postprandial lipaemia, glucose metabolism, CRP and adiponectin.


2002 ◽  
Vol 39 ◽  
pp. 253-254
Author(s):  
Wei-Chuan Tsai ◽  
Yi-Heng Li ◽  
Chih-Chan Lin ◽  
Ting-Hsing Chao ◽  
Jyh-Hong Chen

2005 ◽  
Vol 94 (5) ◽  
pp. 791-795 ◽  
Author(s):  
Annika Smedman ◽  
Samar Basu ◽  
Stefan Jovinge ◽  
Gunilla Nordin Fredrikson ◽  
Bengt Vessby

We previously showed that conjugated linoleic acid (CLA) increases 15-keto-dihydro-prostaglandin F2α, a marker for cyclooxygenase-mediated lipid peroxidation and thus an indicator of cyclooxygenase-mediated inflammation. The aim of the present study was to investigate the effects of CLA on other indicators of inflammation in human subjects, including C-reactive protein, TNF-α, TNF-α receptors 1 and 2, and vascular cell adhesion molecule-1. In a double-blind, placebo-controlled study, fifty-three human subjects were supplemented with a mixture (4·2g/d) of the isomers cis-9,trans-11 CLA and trans-10,cis-12 CLA or control oil for 3 months. CLA supplementation increased levels of C-reactive protein (P=0·003) compared with the control group. However, no changes in TNF-α, TNF-α receptors 1 and 2, and vascular cell adhesion molecule-1 were detected.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Kristine C. Y. McGrath ◽  
Xiao-Hong Li ◽  
Lucinda S. McRobb ◽  
Alison K. Heather

Oxidative stress and inflammation, leading to endothelial dysfunction, contribute to the pathogenesis of atherosclerosis. The popularity of natural product supplements has increased in recent years, especially those with purported anti-inflammatory and/or antioxidant effects. The efficacy and mechanism of many of these products are not yet well understood. In this study, we tested the antioxidant and anti-inflammatory effects of a supplement, HIPER Health Supplement (HIPER), on cytokine-induced inflammation and oxidative stress in human coronary artery endothelial cells (HCAECs). HIPER is a mixture of French maritime pine bark extract (PBE), honey, aloe vera, and papaya extract. Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression. HIPER inhibited TNF-αinduced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation. Further investigation of mechanism showed HIPER reduced TNF-αinduced IκBαand p38 and MEK1/2 MAP kinases phosphorylation. Our findings show that HIPER has potent inhibitory effects on HCAECs inflammatory and oxidative stress responses that may protect against endothelial dysfunction that underlies early atherosclerotic lesion formation.


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