Hotez P J, Le Trang N, Fairlamb A H, Cerami A
Parasite Immunol. 1984 May;6(3):203-9. doi: 10.1111/j.1365-3024.1984.tb00793.x.
Lysates of the haematoprotozoa Trypanosoma brucei or Plasmodium berghei stimulated murine peritoneal exudate cells to release a mediator, which suppressed lipoprotein lipase activity in differentiating 3T3-L1 preadipocytes. The parasite-induced mediator suppressed the activity of cell surface lipoprotein lipase up to 39% in a dose dependent manner. By impairing the activity of cell surface lipoprotein lipase, this mediator acts to inhibit the uptake of fatty acid, and ultimately the accumulation of lipid by the adipocyte. In vivo this defect in triglyceride removal may explain the hypertriglyceridemia commonly observed in haematoprotozoan infections. We suggest that the lipoprotein lipase suppression mediator is produced as a consequence of the immune response to these parasitic protozoa.
血液原生动物布氏锥虫或伯氏疟原虫的裂解物刺激小鼠腹腔渗出细胞释放一种介质，该介质可抑制分化中的3T3-L1前脂肪细胞中的脂蛋白脂肪酶活性。寄生虫诱导的介质以剂量依赖的方式将细胞表面脂蛋白脂肪酶的活性抑制高达39%。通过损害细胞表面脂蛋白脂肪酶的活性，这种介质可抑制脂肪酸的摄取，并最终抑制脂肪细胞中脂质的积累。在体内，甘油三酯清除的这种缺陷可能解释了血液原生动物感染中常见的高甘油三酯血症。我们认为，脂蛋白脂肪酶抑制介质是对这些寄生原生动物免疫反应的结果。
