Nassir F, Mazur A, Gueux E, Sérougne C, Rayssiguier Y
Centre de Recherches en Nutrition Humaine, Laboratoire des Maladies Métaboliques, INRA, St. Genès Champanelle, France.
Lipids. 1994 Oct;29(10):727-9. doi: 10.1007/BF02538918.
Copper deficiency induces hypercholesterolemia in the rat. This hypercholesterolemia is mainly due to an increase in apo E-rich high density lipoproteins (HDL1). The present study was undertaken to determine whether the HDL increase could be explained by altered low-molecular weight apolipoprotein (apo) synthesis in the liver. The effect of copper deficiency on apo A-I, apo A-IV and apo E concentrations in plasma, as well as on respective mRNA levels and synthesis in the liver, were therefore investigated. We observed that the increased HDL1 levels in the plasma of copper-deficient rats were associated with a significant rise in plasma apo E concentrations; however, plasma apo A-I and apo A-IV concentrations remained unchanged. Liver apo synthesis and respective apo mRNA levels were not significantly altered in copper-deficient animals when compared to control rats. No changes in apo E mRNA levels in various tissues from copper-deficient, as compared to control rats, were noted. Based on the data obtained, it was concluded that the observed changes in plasma lipoprotein and apo concentrations are not related to changes in low-molecular weight apo synthesis in the liver. The mechanisms of the impaired catabolism of HDL1 should be further evaluated to possibly explain the observed increase in this fraction in copper-deficient rats.
铜缺乏会诱发大鼠出现高胆固醇血症。这种高胆固醇血症主要归因于富含载脂蛋白E的高密度脂蛋白（HDL1）增加。本研究旨在确定HDL增加是否可以通过肝脏中低分子量载脂蛋白（apo）合成的改变来解释。因此，研究了铜缺乏对血浆中载脂蛋白A-I、载脂蛋白A-IV和载脂蛋白E浓度的影响，以及对肝脏中各自mRNA水平和合成的影响。我们观察到，铜缺乏大鼠血浆中HDL1水平升高与血浆载脂蛋白E浓度显著升高相关；然而，血浆载脂蛋白A-I和载脂蛋白A-IV浓度保持不变。与对照大鼠相比，铜缺乏动物的肝脏载脂蛋白合成和各自的载脂蛋白mRNA水平没有显著改变。与对照大鼠相比，未观察到铜缺乏大鼠各种组织中载脂蛋白E mRNA水平的变化。根据获得的数据得出结论，观察到的血浆脂蛋白和载脂蛋白浓度变化与肝脏中低分子量载脂蛋白合成的变化无关。HDL1分解代谢受损的机制应进一步评估，以可能解释在铜缺乏大鼠中观察到的该部分升高。
