Ghosh P, Chirtel S J, Lakshman M R
Lipid Research Laboratory, V.A. Medical Center, Washington, DC 20422.
Alcohol Clin Exp Res. 1991 Aug;15(4):725-9. doi: 10.1111/j.1530-0277.1991.tb00586.x.
We have previously shown in rats that chronic ethanol feeding significantly inhibits the incorporation of labeled leucine into Apo E secreted into the liver perfusate (p less than 0.01). Fish oil has been shown to counteract many of the adverse effects of ethanol. In order to explore whether this inhibitory effect of ethanol was due to the decreased synthesis and/or defective glycosylation of this glycoprotein, we have determined the effects of chronic ethanol and fish oil on the synthesis and glycosylation of Apo E in vivo. Four groups of male Wistar rats were pair-fed the following liquid diets for 8 weeks; (1) Ethanol Regular Fat, (2) Control Regular Fat, (3) Ethanol Fish Oil, and (4) Control Fish Oil. At the end, the rats were intraportally injected with a single dose of [U-14C]leucine (0.2 microCi/g body weight) and/or [2-3H]mannose (1 microCi/g body weight) and killed after 30 min. The incorporation of the labeled precursors into the immunoprecipitable Apo E was measured in the liver and its microsomal and Golgi fractions. The results showed marked decreases in mannose incorporation into total glycoproteins and specifically of Apo E in whole liver, microsomal, and Golgi fractions under ethanol treatment. In contrast, the leucine incorporation into liver Apo E increased 11% (p less than 0.048) by ethanol treatment. As a result, the [3H]mannose/[14C] leucine incorporation ratio also decreased 41% to 47% at the whole liver, microsomal, and Golgi fractions indicating a marked inhibition in glycosylation of Apo E in the ethanol group.(ABSTRACT TRUNCATED AT 250 WORDS)
我们之前在大鼠身上发现，长期喂食乙醇会显著抑制标记的亮氨酸掺入肝脏灌流液中分泌的载脂蛋白E（Apo E）（p<0.01）。鱼油已被证明可抵消乙醇的许多不良影响。为了探究乙醇的这种抑制作用是否是由于该糖蛋白合成减少和/或糖基化缺陷，我们确定了长期喂食乙醇和鱼油对体内Apo E合成和糖基化的影响。四组雄性Wistar大鼠成对喂食以下液体饮食8周：（1）乙醇常规脂肪组，（2）对照常规脂肪组，（3）乙醇鱼油组，（4）对照鱼油组。最后，给大鼠门静脉内注射单剂量的[U-14C]亮氨酸（0.2微居里/克体重）和/或[2-3H]甘露糖（1微居里/克体重），30分钟后处死。在肝脏及其微粒体和高尔基体部分测量标记前体掺入可免疫沉淀的Apo E中的情况。结果显示，在乙醇处理下，整个肝脏、微粒体和高尔基体部分中，甘露糖掺入总糖蛋白以及特别是Apo E的量显著减少。相比之下，乙醇处理使肝脏Apo E中的亮氨酸掺入量增加了11%（p<0.048）。因此，在整个肝脏、微粒体和高尔基体部分，[3H]甘露糖/[14C]亮氨酸掺入率也降低了41%至47%，表明乙醇组中Apo E的糖基化受到显著抑制。（摘要截短于250字）
