Betteridge D J, Krone W, Ford J M, Galton D J
Eur J Clin Invest. 1979 Dec;9(6):439-41. doi: 10.1111/j.1365-2362.1979.tb00909.x.
Leucocytes from normal subjects and from patients with acute myeloblastic leukaemia incubated for 9 h in the absence of lipoproteins increased their rate of sterol biosynthesis from [2-14C]acetate threefold. Subsequent addition of complete serum, low density lipoprotein or cholesterol in a non-lipoprotein form suppressed sterol synthesis in leucocytes from normal subjects. In contrast, complete serum or low density lipoprotein totally failed to suppress sterol synthesis in leukaemic blast cells. However, when these cells were incubated with cholesterol in a non-lipoprotein form suppression of sterol synthesis occurred as in normal leucocytes. These results suggest that leukaemic blast cells behave like cells from patients with familial hypercholesterolaemia in showing failure of regulation of sterol synthesis by low density lipoprotein.
正常受试者及急性髓细胞白血病患者的白细胞在无脂蛋白条件下孵育9小时后，其从[2-¹⁴C]乙酸盐合成固醇的速率提高了三倍。随后添加完全血清、低密度脂蛋白或非脂蛋白形式的胆固醇可抑制正常受试者白细胞中的固醇合成。相比之下，完全血清或低密度脂蛋白完全无法抑制白血病原始细胞中的固醇合成。然而，当这些细胞与非脂蛋白形式的胆固醇一起孵育时，固醇合成受到抑制，情况与正常白细胞相同。这些结果表明，白血病原始细胞的行为类似于家族性高胆固醇血症患者的细胞，表现为低密度脂蛋白对固醇合成的调节失效。
