Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis.
Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis.
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代谢综合征中的内皮脂肪酶浓度增加，并与冠状动脉粥样硬化有关。
DOI：
10.1371/journal.pmed.0030022
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发表时间：
2006-02
期刊：
影响因子：
15.8
通讯作者：
Rader, DJ
中科院分区：
文献类型：
--
作者：
Badellino, KO;Wolfe, ML;Reilly, MP;Rader, DJ
内皮脂酶（EL）是脂酶家族的一个新成员，在小鼠模型中已被证明可调节高密度脂蛋白（HDL-C）代谢和动脉粥样硬化。我们假设EL浓度与人类HDL-C降低和动脉粥样硬化增加有关。招募有早发冠心病家族史的健康个体（n = 858）作为动脉粥样硬化遗传风险研究的一部分。在单次静脉肝素给药前和给药后，在一个亚组（n = 510）中空腹采血。酶法测定血脂，核磁共振评估脂蛋白亚类，电子束计算机断层扫描定量冠状动脉钙化（CAC）。血浆EL质量测定使用新开发的酶联免疫吸附试验。肝素给药前血浆中的中位EL质量为442（四分位距= 324-617）ng/ml。肝素后中位质量约高3倍，为1，313（888- 1，927）ng/ml。肝素前EL质量和肝素后EL质量之间的相关性为0.46（p < 0.001）。肝素治疗前和治疗后血浆中的EL质量浓度与所有NCEP ATPIII定义的代谢综合征因素显着相关：腰围（r分别为0.28和0.22，p < 0.001），血压（r = 0.18和0.24，p < 0.001），甘油三酯（r = 0.22，p < 0.001;和0.13，p = 0.004），HDL胆固醇（r =-0.11，p = 0.002;和-0.18，p < 0.001）和空腹血糖（r = 0.11和0.16，p = 0.001）。常规（比值比[OR] = 1.67，p = 0.01）和肝素后（OR = 2.42，p = 0.003）血浆中的EL质量与CAC相关，这是通过调整年龄、性别、腰围、血管活性药物、激素替代治疗（女性）和确定的心血管危险因素后的有序回归确定的。据我们所知，我们首次报告，人血浆EL浓度，肝素后和常规肝素前血浆，与代谢综合征的特点和亚临床动脉粥样硬化显着相关。EL可能是人类的促动脉粥样硬化因子，特别是在超重个体和代谢综合征患者中。啮齿类动物的研究表明，内皮脂肪酶可能在动脉粥样硬化的发展中发挥作用。这项研究发现了EL水平和人类早期动脉粥样硬化之间的关联。
Endothelial lipase (EL), a new member of the lipase family, has been shown to modulate high-density lipoprotein (HDL-C) metabolism and atherosclerosis in mouse models. We hypothesized that EL concentrations would be associated with decreased HDL-C and increased atherosclerosis in humans. Healthy individuals with a family history of premature coronary heart disease (n = 858) were recruited as part of the Study of the Inherited Risk of Atherosclerosis. Blood was drawn in the fasting state before and, in a subgroup (n = 510), after administration of a single dose of intravenous heparin. Plasma lipids were measured enzymatically, lipoprotein subclasses were assessed by nuclear magnetic resonance, and coronary artery calcification (CAC) was quantified by electron beam computed tomography. Plasma EL mass was measured using a newly developed enzyme-linked immunosorbent assay. Median EL mass in pre-heparin plasma was 442 (interquartile range = 324–617) ng/ml. Median post-heparin mass was approximately 3-fold higher, 1,313 (888–1,927) ng/ml. The correlation between pre-heparin EL mass and post-heparin EL mass was 0.46 (p < 0.001). EL mass concentrations in both pre- and post-heparin plasma significantly correlated with all NCEP ATPIII-defined metabolic syndrome factors: waist circumference (r = 0.28 and 0.22, respectively, p < 0.001 for each), blood pressure (r = 0.18 and 0.24, p < 0.001 for each), triglycerides (r = 0.22, p < 0.001; and 0.13, p = 0.004), HDL cholesterol (r = –0.11, p = 0.002; and –0.18, p < 0.001), and fasting glucose (r = 0.11 and 0.16, p = 0.001 for both). EL mass in both routine (odds ratio [OR] = 1.67, p = 0.01) and post-heparin (OR = 2.42, p = 0.003) plasma was associated with CAC as determined by ordinal regression after adjustment for age, gender, waist circumference, vasoactive medications, hormone replacement therapy (women), and established cardiovascular risk factors. We report, to our knowledge for the first time, that human plasma EL concentrations, in both post-heparin and routine pre-heparin plasma, are significantly associated with metabolic syndrome features and with subclinical atherosclerosis. EL may be a pro-atherogenic factor in humans, especially in overweight individuals and those with metabolic syndrome. Studies in rodents had suggested that endothelial lipase might play a role in the development of atherosclerosis. This study finds an association between EL levels and early-stage atherosclerosis in humans.
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影响因子：
20.3
作者：
De Geest, BR;Van Linthout, SA;Collen, D
通讯作者：
Collen, D
影响因子：
5
作者：
Hokanson, JE;Kamboh, MI;Hamman, RF
通讯作者：
Hamman, RF
DOI：
10.1016/0735-1097(90)90282-t
发表时间：
1990-03-15
影响因子：
24
作者：
AGATSTON, AS;JANOWITZ, WR;DETRANO, R
通讯作者：
DETRANO, R
影响因子：
16.2
作者：
Bonora, E;Saggiani, F;Muggeo, M
通讯作者：
Muggeo, M
影响因子：
4.8
作者：
Hirata, K;Dichek, HL;Quertermous, T
通讯作者：
Quertermous, T