ABNORMALITIES IN VERY LOW, LOW, AND HIGH-DENSITY LIPOPROTEINS IN HYPERTRIGLYCERIDEMIA - REVERSAL TOWARD NORMAL WITH BEZAFIBRATE TREATMENT
ABNORMALITIES IN VERY LOW, LOW, AND HIGH-DENSITY LIPOPROTEINS IN HYPERTRIGLYCERIDEMIA - REVERSAL TOWARD NORMAL WITH BEZAFIBRATE TREATMENT
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DOI：
10.1172/jci111444
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发表时间：
1984-01-01
影响因子：
15.9
通讯作者：
DECKELBAUM, RJ
中科院分区：
文献类型：
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作者：
EISENBERG, S;GAVISH, D;DECKELBAUM, RJ
在16名高胆固醇血症（HTG）受试者（222-2500 mg/dl）中研究了苯扎贝特治疗开始前后胆固醇血症对血浆脂蛋白的影响。苯扎贝特使血浆甘油三酯平均降低56%，使脂蛋白和肝甘油三酯脂肪酶水平分别升高260%和213%。测定了极低密度脂蛋白（VLDL）的性质，在血浆密度和低密度脂蛋白和高密度脂蛋白（LDL和HDL），分离的带状超离心，分离。HTG-LDL表现为多组分，而HTG-HDL主要表现为HDL 3。HTG-VLDL的载脂蛋白和甘油三酯相对较少，但富含游离胆固醇和酯化胆固醇。HTG-LDL（主要组分）缺乏游离和酯化胆固醇，但富含脱辅基蛋白和甘油三酯。它也比正常情况下更密集和更小。HTG-HDL 3比N-HDL 3密度更大，并且表现出与HTG-LDL相似的压缩异常。随着VLDL质量的减少，异常恢复正常。这伴随着LDL-载脂蛋白B和胆固醇水平的增加，这表明VLDL向LDL的转化增加。显示了血浆甘油三酯与所有异常程度之间的显著相关性。治疗期间获得的数据证实了这些关系。显然，大多数异常反映了糖尿病的程度。显然，血浆核心脂质转移蛋白是异常胆固醇酯分布的效应物。它对越来越大和代谢缓慢的VLDL群体的长期作用将导致相应的胆固醇酯向VLDL和甘油三酯向LDL和HDL的过度转移。据计算，在中度HTG中，LDL和HDL仅含有正常胆固醇负荷的50%。HTG中的胆固醇酯再分布可能对调节代谢事件很重要。
The effects of triglyceridemia on plasma lipoproteins were investigated in 16 hypertriglyceridemic (HTG) subjects (222-2500 mg/dl) before and after the initiation of bezafibrate therapy. Bezafibrate caused a mean reduction of 56% in plasma triglyceride and increased the levels of lipoprotein and hepatic triglyceride lipases by 260 and 213%, respectively. The natures of very low density lipoprotein (VLDL), isolated at plasma density and of low and high density lipoprotein (LDL and HDL), separated by zonal ultracentrifugation, were determined. HTG-LDL appears as multiple fraction whereas HTG-HDL is seen predominantly as HDL3. HTG-VLDL is relatively poor in apoproteins and triglycerides but enriched in free and esterified cholesterol. HTG-LDL (main fraction) is depleted of free and esterified cholesterol but enriched in apoprotein and triglyceride. It is also denser and smaller than normal. HTG-HDL3 is denser than N-HDL3 and demonstrates compsitional abnormalities similar to those of HTG-LDL. With the reduction of the VLDL mass, abnormalties revert towards normal. This is accompanied by an increase in LDL-apoprotein B and cholesterol levels, which indicates an increased conversion of VLDL to LDL. Significant corelations between plasma triglyceride and the degree of all abnormalities are shown. The data obtained during treatment corroborate these relationships. Evidently most abnormalities reflect the degree of triglyceridemia. Apparently plasma core-lipid transfer protein(s) is an effector of the abnormal cholesteryl ester distribution. Its prolonged action on increasingly large and slowly metabolized VLDL populations would entail a correspondingly excessive transfer of cholesteryl ester to VLDL and of triglyceride to LDL and HDL. It is a calculated that, in moderate HTG, LDL and HDL contain only 50% of the normal cholesterol load. Cholesteryl ester redistribution in HTG Might be important in regulating metabolic events.