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【文摘发布】非诺贝特治疗对高甘油三酸酯血症
Author：Robert S. Rosenson, David A. Wolff, Anna L. Huskin, Irene B. Helenowski, and Alfred W. Rademaker
Resource: Diabetes Care 2007 30: 1945-1951.
Abstract：
Objectives The aim of this study was to determine the effects of fenofibrate (160 mg/d) 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 (>/=1.7 mmol/L and <6.9 mmol/L) and two or more of the Adult Treatment Panel III criteria of the metabolic syndrome were randomized to fenofibrate (160 mg/d) or placebo in a double-blind controlled clinical trial.
Results Fenofibrate treatment lowered fasting triglycerides (-46.1%, p<0.0001) and postprandial (area under the curve) triglycerides (-45.4%, p<0.0001) due to significant reductions in postprandial levels of large (-40.8%, p<0.0001) and medium (-49.5%, p<0.0001) very low-density lipoprotein (VLDL) particles. Fasting total low-density lipoprotein (LDL) particle number was reduced in fenofibrate treated subjects (-19.0%, p = 0.0033) due primarily to reductions in small LDL particles (-40.3%, p<0.0001); these treatment differences persisted postprandial. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared to placebo (-15.3%, p = 0.0013 and 31.0%, p<0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble VCAM-1 (-10.9%, p = 0.0005 and -12.0%, p = 0.0001, respectively) as well as fasting and postprandial soluble ICAM-1 (-14.8%, p<0.0001 and -15.3%, p<0.0001, respectively). Reduction in VCAM-1 and ICAM-1 was correlated with reductions in fasting and postprandial large VLDL particles (p<0.0001) as well as postprandial oxidized fatty acids (p<0.0005).
Conclusions Triglyceride-lowering therapy with fenofibrate reduced fasting and postprandial free fatty acid oxidation and inflammatory responses, and these anti-atherosclerotic effects were most highly correlated with reductions in large VLDL particles.
PMID: 17483155 Title：Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome
标题：非诺贝特治疗对高甘油三酯血症和代谢综合征患者空腹及餐后脂蛋白血症、氧化应激与炎症反应的改善作用
Abstract：
Objectives The aim of this study was to determine the effects of fenofibrate (160 mg/d) on fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediators in subjects with hypertriglyceridemia and the metabolic syndrome.
摘要:
目的 本研究旨在确定非诺贝特治疗(160毫克/日)对高甘油三酯血症和代谢综合征患者空腹及餐后脂蛋白血症、氧化的脂肪酸与炎症介质的作用。
Research Design and Methods Fifty-nine subjects with fasting hypertriglyceridemia (>/=1.7 mmol/L and <6.9 mmol/L) and two or more of the Adult Treatment Panel III criteria of the metabolic syndrome were randomized to fenofibrate (160 mg/d) or placebo in a double-blind controlled clinical trial.
研究设计和方法 这项双盲对照临床试验共纳入59名患者，均有空腹高甘油三酯血症(>/=1.7mmol/L但<6.9mmol/L)，并有成人治疗小组（ATP III）代谢综合征定义中的2条以上代谢异常，将患者随机分为2组，分别接受非诺贝特(160毫克/日)或安慰剂治疗。
Results Fenofibrate treatment lowered fasting triglycerides (-46.1%, p<0.0001) and postprandial (area under the curve) triglycerides (-45.4%, p<0.0001) due to significant reductions in postprandial levels of large (-40.8%, p<0.0001) and medium (-49.5%, p<0.0001) very low-density lipoprotein (VLDL) particles. Fasting total low-density lipoprotein (LDL) particle number was reduced in fenofibrate treated subjects (-19.0%, p = 0.0033) due primarily to reductions in small LDL particles (-40.3%, p<0.0001); these treatment differences persisted postprandial. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared to placebo (-15.3%, p = 0.0013 and 31.0%, p<0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble VCAM-1 (-10.9%, p = 0.0005 and -12.0%, p = 0.0001, respectively) as well as fasting and postprandial soluble ICAM-1 (-14.8%, p<0.0001 and -15.3%, p<0.0001, respectively). Reduction in VCAM-1 and ICAM-1 was correlated with reductions in fasting and postprandial large VLDL particles (p<0.0001) as well as postprandial oxidized fatty acids (p<0.0005).
结果 由于非诺贝特治疗明显降低了餐后大(-40.8%，p<0.0001)和中等大小(-49.5%,p<0.0001)极低密度脂蛋白(VLDL)水平，从而降低了空腹(-46.1%, p<0.0001)和餐后(-45.4%, p<0.0001)甘油三酯(曲线下面积)。因为非诺贝特治疗降低了小的低密度脂蛋白(LDL)微粒数(-40.3%, p<0.0001)，因此空腹总LDL微粒数减少(-19.0%,p=0.0033)，该作用在餐后LDL中有差异。非诺贝特组较安慰剂组降低了空腹和餐后氧化脂肪酸水平(-15.3%,p=0.0013和31.0%,p<0.0001)，降低了空腹和餐后可溶性血管细胞粘附分子-1(VCAM-1)(-10.9%,p=0.0005和-12.0%, p=0.0001)，降低了空腹和餐后可溶性细胞间粘附分子-1(ICAM-1)(-14.8%, p<0.0001和-15.3%, p<0.0001)。VCAM-1和ICAM-1的降低和空腹与餐后大VLDL颗粒减少、餐后氧化脂肪酸降低有关。
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作者:admin@医学,生命科学 2011-07-09 17:11
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