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

被引:148
作者
Tsai, WC [1 ]
Li, YH [1 ]
Lin, CC [1 ]
Chao, TH [1 ]
Chen, JH [1 ]
机构
[1] Natl Cheng Kung Univ, Div Cardiol, Dept Internal Med, Med Ctr, Tainan 70101, Taiwan
关键词
endothelial function; flow-mediated vasodilatation; glutathione peroxidase; high-fat meal; oxidative stress; postprandial hypertriglyceridaemia;
D O I
10.1042/CS20030227
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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 F-2alpha (8-PGF(2alpha)), a free radical-catalysed product from the oxidative modification of arachiclonic 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-I and vascular cell-adhesion molecule-I were also measured. High-resolution ultrasound was used to assess the flowmediated 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 mug/ml to 25.7 +/- 11.8 mug/ml (P = 0.022) 2 h after the meal, and urinary excretion of 8-PGF(2alpha) significantly increased from 1286 +/- 1401 pg/mg of creatinine to 2 197 +/- 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.
引用
收藏
页码:315 / 319
页数:5
相关论文
共 33 条
[1]   Soluble cell adhesion molecules in hypertriglyceridemia and potential significance on monocyte adhesion [J].
Abe, Y ;
El-Masri, B ;
Kimball, KT ;
Pownall, H ;
Reilly, CF ;
Osmundsen, K ;
Smith, CW ;
Ballantyne, CM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (05) :723-731
[2]   The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes [J].
Anderson, RA ;
Evans, ML ;
Ellis, GR ;
Graham, J ;
Morris, K ;
Jackson, SK ;
Lewis, MJ ;
Rees, A ;
Frenneaux, MP .
ATHEROSCLEROSIS, 2001, 154 (02) :475-483
[3]   Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress [J].
Bae, JH ;
Bassenge, E ;
Kim, KB ;
Kim, YN ;
Kim, KS ;
Lee, HJ ;
Moon, KC ;
Lee, MS ;
Park, KY ;
Schwemmer, M .
ATHEROSCLEROSIS, 2001, 155 (02) :517-523
[4]   NONINVASIVE DETECTION OF ENDOTHELIAL DYSFUNCTION IN CHILDREN AND ADULTS AT RISK OF ATHEROSCLEROSIS [J].
CELERMAJER, DS ;
SORENSEN, KE ;
GOOCH, VM ;
SPIEGELHALTER, DJ ;
MILLER, OI ;
SULLIVAN, ID ;
LLOYD, JK ;
DEANFIELD, JE .
LANCET, 1992, 340 (8828) :1111-1115
[5]   Ciprofibrate therapy improves endothelial function and reduces postprandial lipemia and oxidative stress in type 2 diabetes mellitus [J].
Evans, M ;
Anderson, RA ;
Graham, J ;
Ellis, GR ;
Morris, K ;
Davies, S ;
Jackson, SK ;
Lewis, MJ ;
Frenneaux, MP ;
Rees, A .
CIRCULATION, 2000, 101 (15) :1773-1779
[6]   Pronounced postprandial lipemia impairs endothelium-dependent dilation of the brachial artery in men [J].
Gaenzer, H ;
Sturm, W ;
Neumayr, G ;
Kirchmair, R ;
Ebenbichler, C ;
Ritsch, A ;
Föger, B ;
Weiss, G ;
Patsch, JR .
CARDIOVASCULAR RESEARCH, 2001, 52 (03) :509-516
[7]  
GUEMOURI L, 1991, CLIN CHEM, V37, P1932
[8]   Levels of soluble cell adhesion molecules in patients with dyslipidemia [J].
Hackman, A ;
Abe, Y ;
Insull, W ;
Pownall, H ;
Smith, L ;
Dunn, K ;
Gotto, AM ;
Ballantyne, CM .
CIRCULATION, 1996, 93 (07) :1334-1338
[9]   Biological mechanisms for the clinical success of lipid-lowering in coronary artery disease and the use of surrogate end-points [J].
Kinlay, S ;
Selwyn, AP ;
Delagrange, D ;
Creager, MA ;
Libby, P ;
Ganz, P .
CURRENT OPINION IN LIPIDOLOGY, 1996, 7 (06) :389-397
[10]   Glutathione-related antioxidant defenses in human atherosclerotic plaques [J].
Lapenna, D ;
de Gioia, S ;
Ciofani, G ;
Mezzetti, A ;
Ucchino, S ;
Calafiore, AM ;
Napolitano, AM ;
Di Ilio, C ;
Cuccurullo, F .
CIRCULATION, 1998, 97 (19) :1930-1934