Mechanisms by which saturated triacylglycerols elevate the plasma low density lipoprotein-cholesterol concentration in hamsters. Differential effects of fatty acid chain length.
Mechanisms by which saturated triacylglycerols elevate the plasma low density lipoprotein-cholesterol concentration in hamsters. Differential effects of fatty acid chain length.
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饱和三酰甘油提高仓鼠血浆低密度脂蛋白胆固醇浓度的机制。
DOI：
10.1172/jci114131
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Dietschy,JM
中科院分区：
文献类型：
--
作者：
Woollett,LA;Spady,DK;Dietschy,JM
这些研究旨在阐明较短（MCT）和较长（HCO）链长的饱和三酰甘油和胆固醇如何相互作用以改变稳态血浆LDL-胆固醇水平。当在不存在胆固醇的情况下饲喂MCT或HCO时，对受体依赖性LDL转运几乎没有影响，但LDL-胆固醇产生增加36-43%。在不存在三酰甘油的情况下喂食胆固醇导致受体依赖性LDL转运的显著抑制和LDL-胆固醇产生的26-31%增加。然而，当长链饱和三酰甘油与胆固醇一起喂养时，受体依赖性LDL转运的抑制显着增加，生产率增加82%。总之，这两种变化导致观察到的血浆LDL-胆固醇浓度增加8倍。相比之下，喂食较短链长的饱和三酰甘油与胆固醇实际上增强了受体依赖性LDL转运，同时也导致LDL-胆固醇产生率的小幅增加（52%）。由于这两个相反的事件，MCT喂养对血浆LDL-胆固醇水平基本上没有超出胆固醇单独喂养诱导的净影响。
These studies were designed to elucidate how shorter (MCT) and longer (HCO) chain-length saturated triacylglycerols and cholesterol interact to alter steady-state plasma LDL-cholesterol levels. When either MCT or HCO was fed in the absence of cholesterol, there was little effect on receptor-dependent LDL transport but a 36-43% increase in LDL-cholesterol production. Cholesterol feeding in the absence of triacylglycerol led to significant suppression of receptor-dependent LDL transport and a 26-31% increase in LDL-cholesterol production. However, when the longer chain-length saturated triacylglycerol was fed together with cholesterol there was a marked increase in the suppression of receptor-dependent LDL transport and an 82% increase in production rate. Together, these two alterations accounted for the observed eightfold increase in plasma LDL-cholesterol concentration. In contrast, feeding the shorter chain-length saturated triacylglycerol with cholesterol actually enhanced receptor-dependent LDL transport while also causing a smaller increase (52%) in the LDL-cholesterol production rate. As a result of these two opposing events, MCT feeding had essentially no net effect on plasma LDL-cholesterol levels beyond that induced by cholesterol feeding alone.