Nassir F, Mazur A, Sérougne C, Gueux E, Rayssiguier Y
Laboratoire des Maladies Métaboliques, INRA, Theix, St. Gènes Champanelle, France.
FEBS Lett. 1993 May 3;322(1):33-6. doi: 10.1016/0014-5793(93)81105-9.
The present study was designed to examine if induction of apolipoprotein B synthesis is associated with hypercholesterolemia in copper-deficient rats. This hypercholesterolemia mainly resides in an increase in the HDL-1 and LDL and is associated with a significant increase in plasma apoB concentration. Liver apoB mRNA levels were not significantly modified in deficient animals as compared to control rats. Studies on liver apolipoprotein synthesis indicated that apoB100 synthesis was increased in deficient animals whereas apoB48 synthesis was unchanged. Thus, it appears that the increase in apoB synthesis in the liver of copper-deficient rats occurs at the posttranscriptional level. The selective increase in apoB100 synthesis indicates the possible impact of this deficiency on the editing of apoB. An increase in apoB100 synthesis by the liver in copper-deficient rats may significantly contribute to the increase in plasma concentration of LDL.
本研究旨在探讨载脂蛋白B合成的诱导是否与铜缺乏大鼠的高胆固醇血症有关。这种高胆固醇血症主要表现为HDL-1和LDL增加,并与血浆载脂蛋白B浓度的显著升高有关。与对照大鼠相比,缺乏铜的动物肝脏载脂蛋白B mRNA水平没有显著改变。对肝脏载脂蛋白合成的研究表明,缺乏铜的动物中apoB100合成增加,而apoB48合成没有变化。因此,铜缺乏大鼠肝脏中载脂蛋白B合成的增加似乎发生在转录后水平。apoB100合成的选择性增加表明这种缺乏可能对apoB的编辑产生影响。铜缺乏大鼠肝脏中apoB100合成的增加可能显著导致血浆LDL浓度的升高。