Nassir F, Giannoni F, Mazur A, Rayssiguier Y, Davidson N O
Laboratoire des Maladies Metaboliques, INRA, Theix, St Genes Champanelle, France.
Lipids. 1996 Apr;31(4):433-6. doi: 10.1007/BF02522931.
Experimentally induced copper deficiency in the rat results in increased plasma apolipoprotein B100 (apo B100) concentration in association with increased hepatic apo B100 synthesis. This enhancement of apo B100 synthesis and plasma accumulation accounts for the rise of plasma low density lipoprotein in these animals. In the present study, we have investigated if the selective increase in hepatic apo B100 synthesis is accounted for by changes in apo B mRNA editing. Reverse transcription coupled with polymerase chain reaction amplification and primer extension analysis of apo B cDNA revealed no differences in apo B mRNA editing in either the liver or small intestine between control and copper-deficient rats. We speculate that the increase in apo B100 synthesis in the liver of copper-deficient rats reflects posttranslational alterations in gene expression accompanying changes in very low density lipoprotein assembly and secretion.
实验诱导大鼠铜缺乏会导致血浆载脂蛋白B100（apo B100）浓度升高，同时肝脏apo B100合成增加。apo B100合成及血浆蓄积的这种增强导致了这些动物血浆低密度脂蛋白的升高。在本研究中，我们调查了肝脏apo B100合成的选择性增加是否由apo B mRNA编辑的变化所致。对apo B cDNA进行逆转录结合聚合酶链反应扩增及引物延伸分析显示，对照大鼠和铜缺乏大鼠的肝脏或小肠中，apo B mRNA编辑均无差异。我们推测，铜缺乏大鼠肝脏中apo B100合成的增加反映了伴随极低密度脂蛋白组装和分泌变化的基因表达的翻译后改变。
