van Ree J H, Gijbels M J, van den Broek W J, Hofker M H, Havekes L M
TNO Prevention and Health, Gaubius Laboratory, Leiden, The Netherlands.
Atherosclerosis. 1995 Jan 20;112(2):237-43. doi: 10.1016/0021-9150(94)05419-j.
Apolipoprotein (apo) E-deficient mice were fed a hypercholesterolemic diet for 14 weeks. Mean serum cholesterol levels rose to 37.5 mM. Upon complete necroscopy, massive xanthomatous lesions were noticed in various tissues, with a predilection for subcutaneous and peritendinous tissues, while control animals on the same diet (3.4 mM serum cholesterol) and apo E-deficient mice on a regular chow diet (20 mM serum cholesterol) did not show such lesions. Also, apo E3-Leiden transgenic mice fed a high fat diet, with 60 mM of serum cholesterol, did not exhibit any xanthomatosis. The xanthomatous lesions found in the Apoe knock-out mouse clearly differed in location from xanthomas previously found in low density lipoprotein receptor-deficient mice. We conclude that the lack of apo E results in atypical disseminated xanthomatosis, suggesting that apo E has an important role in determining the tissue distribution of cholesterol deposition.
给载脂蛋白（apo）E 缺陷小鼠喂食高胆固醇饮食 14 周。血清胆固醇平均水平升至 37.5 mM。在完整尸检时，在各种组织中发现大量黄色瘤病变，尤其多见于皮下和肌腱周围组织，而相同饮食的对照动物（血清胆固醇 3.4 mM）以及正常饮食的 apo E 缺陷小鼠（血清胆固醇 20 mM）均未出现此类病变。此外，喂食高脂肪饮食且血清胆固醇为 60 mM 的 apo E3 - Leiden 转基因小鼠未表现出任何黄瘤病。在 Apoe 基因敲除小鼠中发现的黄色瘤病变在位置上与先前在低密度脂蛋白受体缺陷小鼠中发现的黄瘤明显不同。我们得出结论，apo E 的缺乏导致非典型播散性黄瘤病，这表明 apo E 在决定胆固醇沉积的组织分布中起重要作用。
