Effects of lovastatin on the levels, structure, and atherogenicity of VLDL in patients with moderate hypertriglyceridemia.
Effects of lovastatin on the levels, structure, and atherogenicity of VLDL in patients with moderate hypertriglyceridemia.
复制标题
洛伐他汀对中度高甘油三酯血症患者 VLDL 水平、结构和致动脉粥样硬化性的影响。
DOI：
10.1161/01.atv.13.4.472
复制
发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Grundy,SM
中科院分区：
文献类型：
--
作者：
Gianturco,SH;Bradley,WA;Nozaki,S;Vega,GL;Grundy,SM
本研究的目的是确定洛伐他汀治疗是否减少高脂血症患者的极低密度脂蛋白（VLDL）异常。洛伐他汀降低血浆甘油三酯水平和总VLDL、中密度脂蛋白（IDL）和低密度脂蛋白（LDL）胆固醇水平。洛伐他汀可减少Sf 100-400和Sf 60-100的VLDL颗粒数量，但不减少Sf 20-60颗粒，每个颗粒的胆固醇酯量也是如此。所有VLDL亚种与培养的人成纤维细胞的LDL受体结合，对安慰剂和洛伐他汀具有相似的高亲和力，但VLDL Sf 100-400和VLDL Sf 60-100在洛伐他汀治疗后对3-羟基-3-甲基戊二酰辅酶A还原酶活性的抑制较小，表明LDL受体介导的胆固醇递送减少。洛伐他汀后VLDL Sf 100-400对还原酶抑制的平均降低为32%，与洛伐他汀后VLDL Sf 100-400的胆固醇酯含量平均降低34%相似。虽然没有达到统计学意义，有一个趋势，减少极低密度脂蛋白Sf 100-400诱导的快速，受体介导的甘油三酯积累在P388 D1巨噬细胞后，洛伐他汀。总而言之，这些观察结果表明，洛伐他汀可能在减少高甘油三酯血症的动脉粥样硬化并发症方面具有潜在益处。
The purpose of this study was to determine whether lovastatin treatment reduced very low density lipoprotein (VLDL) abnormalities in hypertriglyceridemic subjects. Lovastatin reduced plasma triglyceride levels and the levels of total VLDL, intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) cholesterol. The numbers of VLDL particles of Sf 100-400 and Sf 60-100 but not Sf 20-60 particles were reduced by lovastatin, as was the amount of cholesteryl ester per particle. All VLDL subspecies bound to the LDL receptor of cultured human fibroblasts with similar, high affinities on both placebo and lovastatin, but VLDL Sf 100-400 and VLDL Sf 60-100 caused less suppression of 3-hydroxy-3-methyl glutaryl coenzyme A reductase activity after lovastatin therapy, indicating reduced LDL receptor-mediated cholesterol delivery. The average decrease in reductase suppression by VLDL Sf 100-400 after lovastatin was 32%, similar to the 34% average decrease in cholesteryl ester content of VLDL Sf 100-400 after lovastatin. Although statistical significance was not achieved, there was a trend toward decreased VLDL Sf 100-400-induced rapid, receptor-mediated triglyceride accumulation in P388D1 macrophages after lovastatin. Taken together, these observations suggest that lovastatin may be of potential benefit in decreasing the atherosclerotic complications of hypertriglyceridemia.