Hatanaka K, Tanishita H, Ishibashi-Ueda H, Yamamoto A
Biochim Biophys Acta. 1986 Oct 3;878(3):440-5. doi: 10.1016/0005-2760(86)90254-7.
Approximately 70% of the W/WV mice lacking mast cells due to a genetic defect showed hypertriglyceridemia combined with hypercholesterolemia. Increases of various magnitudes in chylomicrons, very-low-density lipoprotein, and intermediate-density lipoprotein were observed in the plasma of W/WV mice compared to those in the plasma of congenic normal mice. The increase in these lipoproteins was seen even in normolipidemic W/WV mice. Activities of both lipoprotein lipase and hepatic triacylglycerol lipase in the plasma after heparin injection were markedly lower in the W/WV mice than in the congenic normal mice, although activities of both lipoprotein lipase in the heart and adipose tissue and hepatic triacylglycerol lipase in the liver were not decreased. These results suggest that the W/WV mice have genetic defects in one or more of the following: secretion of both lipases from their synthesising cells, transport to the endothelium, and anchoring to the endothelial surface. Heparin deficiency in these mice may be responsible for the impairment and, thereby, may partially contribute to the hyperlipidemia.
由于基因缺陷而缺乏肥大细胞的W/WV小鼠中,约70%表现出高甘油三酯血症并伴有高胆固醇血症。与同基因正常小鼠血浆相比,W/WV小鼠血浆中乳糜微粒、极低密度脂蛋白和中间密度脂蛋白有不同程度的增加。即使在血脂正常的W/WV小鼠中也能看到这些脂蛋白的增加。肝素注射后,W/WV小鼠血浆中脂蛋白脂肪酶和肝甘油三酯脂肪酶的活性明显低于同基因正常小鼠,尽管心脏和脂肪组织中的脂蛋白脂肪酶以及肝脏中的肝甘油三酯脂肪酶的活性并未降低。这些结果表明,W/WV小鼠在以下一个或多个方面存在基因缺陷:两种脂肪酶从合成细胞的分泌、向内皮的转运以及在内皮表面的锚定。这些小鼠中肝素缺乏可能是造成这种损害的原因,从而可能部分导致高脂血症。