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Postprnadial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress

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Author(s)
김권배김윤년김기식문교철
Alternative Author(s)
Kim, Kwon BaeKim, Yoon NyunKim, Kee SikMun, Kyo Cheol
Publication Year
2001
Abstract
Aims: it appears that hypertriglyceridemia (HTG) is a risk factor of atherosclerosis as demonstrated by recent studies. In this
study, we analyzed the effects of acute HTG on endothelial function and oxidative stress, which are important mechanisms in the
pathogenesis of atherosclerosis. Methods and results: in a high fat meal group (n 11), serum triglycerides and PMA-activated
leukocyte O2
’ production were significantly (PB0.005) increased from 146969 mg:dl and 4.0990.93 nmol:106 cells:min
preprandially to 198988 mg:dl and 5.4991.19 nmol:106 cells:min, respectively, 2 h after eating a high-fat meal. The
flow-mediated endothelium-dependent brachial artery dilation (FMD; high-resolution ultrasound) was decreased from 13.793.3%
preprandially to 8.293.7%, 2 h after eating a high-fat meal (PB0.005). However, following a low-fat meal (n 9), there were
no significant changes in triglycerides, leukocyte O2
’ production and FMD. Changes of serum triglycerides were correlated
negatively (r 0.650, PB0.005) with changes of FMD, but were correlated positively (r 0.798, PB0.001) with changes of
leukocyte O2
’ production, which — in turn — were correlated negatively (r 0.784, PB0.001) with changes of FMD in all
study subjects (mean age: 56 years, n 20). Conclusions: this study suggests that acute HTG causes endothelial dysfunction via
enhanced oxidant stress and this may pave the way for the development of atherosclerosis under chronic conditions. © 2001
Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Triglyceride; Oxidative stress; Endothelial function
Department
Dept. of Internal Medicine (내과학)
Dept. of Biochemistry (생화학)
Publisher
School of Medicine
Citation
Atheroscleosis, Vol.155(2) : 517-523, 2001
Type
Article
ISSN
0021-9150
DOI
10.1016/S0021-9150(00)00601-8
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35133
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