Al Rifai W, Maurois P, Fruchart J C, Charet P
Biochimie. 1982 Feb;64(2):127-32. doi: 10.1016/s0300-9084(82)80414-8.
Adipose tissue lipoprotein lipase activity (LPL) falls dramatically during experimental infection of mice by Plasmodium chabaudi. The decrease in this activity accounts for the seric accumulation of triacyl-glyceride-rich lipoproteins (chylomicrons mainly and Very Low Density Lipoproteins (VLDL) partly). This loss of tissue LPL enzyme activity is moreover enhanced, in capillary vessels, by a simultaneous decrease in the activatory power of serum towards the enzyme. This phenomenon is mainly related to the presence of Very Low Density Lipoproteins. In the mouse VLDL apoprotein composition is supposed to be modified. On the contrary, in fatal infection of mice by P. vinckei the adipose tissue lipoprotein lipase (LPL) activity is normal or even increased.
在小鼠被恰氏疟原虫实验性感染期间,脂肪组织脂蛋白脂肪酶活性(LPL)急剧下降。该活性的降低导致富含三酰甘油的脂蛋白(主要是乳糜微粒,部分是极低密度脂蛋白(VLDL))在血清中积累。此外,在毛细血管中,血清对该酶的激活能力同时下降,进一步增强了组织LPL酶活性的丧失。这种现象主要与极低密度脂蛋白的存在有关。在小鼠中,VLDL载脂蛋白组成被认为发生了改变。相反,在小鼠被文氏疟原虫致死性感染时,脂肪组织脂蛋白脂肪酶(LPL)活性正常甚至升高。