Dietary fish oil stimulates hepatic low density lipoprotein transport in the rat.

Dietary fish oil stimulates hepatic low density lipoprotein transport in the rat.
复制标题

膳食鱼油刺激大鼠肝脏低密度脂蛋白转运。

DOI:
10.1172/jci114195
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发表时间:
1989
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Spady,DK
Spady,DK
中科院分区:
--
文献类型:
--
作者:
Ventura,MA;Woollett,LA;Spady,DK

文献摘要

被引文献

相似文献

进行这些研究是为了检查鱼油、红花油和氢化椰子油对决定血浆中低密度脂蛋白(LDL)浓度的主要过程的影响,即,LDL产生的速率以及身体各器官中受体依赖性和受体非依赖性LDL摄取的速率。当以20%的水平喂养时,鱼油主要通过增加肝脏中的LDL受体活性将血浆LDL胆固醇水平降低了38%。膳食红花油也增加了肝脏LDL受体活性;然而,由于LDL生成速率也增加,血浆LDL胆固醇水平基本保持不变。氢化椰子油对LDL受体活性没有影响,但增加了LDL-胆固醇产生的速率,导致血浆LDL-胆固醇水平增加46%。膳食鱼油对肝脏无唾液酸胎球蛋白的受体依赖性转运没有影响,表明鱼油对肝脏LDL受体活性的影响是特异性的,而不是由于肝膜物理性质的普遍改变。最后,膳食鱼油增加了肝脏胆固醇酯水平并抑制了肝脏胆固醇合成率,这表明这些动物肝脏LDL受体活性的上调不仅仅是对肝脏胆固醇可用性减少的反应。
These studies were undertaken to examine the effect of fish oil, safflower oil, and hydrogenated coconut oil on the major processes that determine the concentration of low density lipoprotein (LDL) in plasma, i.e., the rate of LDL production and the rates of receptor-dependent and receptor-independent LDL uptake in the various organs of the body. When fed at the 20% level, fish oil reduced plasma LDL-cholesterol levels by 38% primarily by increasing LDL receptor activity in the liver. Dietary safflower oil also increased hepatic LDL receptor activity; however, since the rate of LDL production also increased, plasma LDL-cholesterol levels remained essentially unchanged. Hydrogenated coconut oil had no effect on LDL receptor activity but increased the rate of LDL-cholesterol production causing plasma LDL-cholesterol levels to increase 46%. Dietary fish oil had no effect on the receptor-dependent transport of asialofetuin by the liver, suggesting that the effect of fish oil on hepatic LDL receptor activity was specific and not due to a generalized alteration in the physical properties of hepatic membranes. Finally, dietary fish oil increased hepatic cholesteryl ester levels and suppressed hepatic cholesterol synthesis rates, suggesting that the up-regulation of hepatic LDL receptor activity in these animals was not simply a response to diminished cholesterol availability in the liver.