Howard B V, Egusa G, Beltz W F, Kesäniemi Y A, Grundy S M
J Lipid Res. 1986 Jan;27(1):11-20.
To evaluate factors regulating the concentrations of plasma low density lipoproteins (LDL), apolipoprotein B metabolism was studied in nine Pima Indians (25 +/- 2 yr, 191 +/- 20% ideal wt) with low LDL cholesterol (77 +/- 7 mg/dl) and apoB (60 +/- 4 mg/dl) and in eight age- and weight-matched Caucasians with similar very low density lipoprotein (VLDL) concentrations, but higher LDL (cholesterol = 104 +/- 18; apoB = 82 +/- 10; P less than 0.05). Subjects received autologous 131I-labeled VLDL and 125I-labeled LDL, and specific activities of VLDL-apoB, intermediate density lipoprotein (IDL)-apoB, and LDL-apoB were analyzed using a multicompartmental model. Synthesis of LDL-apoB was similar (1224 +/- 87 mg/d in Pimas vs 1218 +/- 118 mg/d in Caucasians) but in Pimas the fractional catabolic rate (FCR) for LDL-apoB was higher (0.48 +/- 0.02 vs 0.39 +/- 0.04 d-1, P less than 0.05). In the Pimas, a much higher proportion of VLDL-apoB was catabolized without conversion to LDL (47 +/- 3 vs 30 +/- 5%, P less than 0.01). When all subjects were considered together, LDL-apoB concentrations were negatively correlated with both FCR for LDL-apoB (r = -0.79, P less than 0.0001) and the non-LDL pathway (r = -0.43, P less than 0.05). Also, the direct removal (non-LDL) path was correlated with VLDL-apoB production (r = 0.49, P = 0.03), and the direct removal pathway and FCR for LDL-apoB were correlated (r = 0.49, P = 0.03). In conclusion, plasma LDL appear to be regulated by both the catabolism of LDL and the extent of metabolism of VLDL without conversion to LDL; both of these processes may be mediated by the apoB/E receptor, and appear to increase in response to increasing VLDL production.
为评估调节血浆低密度脂蛋白（LDL）浓度的因素，我们对9名皮马印第安人（年龄25±2岁，体重为理想体重的191±20%）和8名年龄及体重匹配的高加索人进行了载脂蛋白B代谢研究。皮马印第安人的LDL胆固醇（77±7mg/dl）和载脂蛋白B（60±4mg/dl）水平较低，高加索人的极低密度脂蛋白（VLDL）浓度与之相似，但LDL水平较高（胆固醇=104±18；载脂蛋白B=82±10；P<0.05）。受试者接受自体131I标记的VLDL和125I标记的LDL，并使用多室模型分析VLDL-载脂蛋白B、中间密度脂蛋白（IDL）-载脂蛋白B和LDL-载脂蛋白B的比活性。LDL-载脂蛋白B的合成相似（皮马人为1224±87mg/d，高加索人为1218±118mg/d），但皮马人LDL-载脂蛋白B的分解代谢率（FCR）较高（0.48±0.02对0.39±0.04d-1，P<0.05）。在皮马人中，未转化为LDL而被分解代谢的VLDL-载脂蛋白B比例更高（47±3对30±5%，P<0.01）。当将所有受试者综合考虑时，LDL-载脂蛋白B浓度与LDL-载脂蛋白B的FCR（r=-0.79，P<0.0001）和非LDL途径（r=-0.43，P<0.05）均呈负相关。此外，直接清除（非LDL）途径与VLDL-载脂蛋白B生成相关（r=0.49，P=0.03），直接清除途径与LDL-载脂蛋白B的FCR也相关（r=0.49，P=0.03）。总之，血浆LDL似乎受LDL分解代谢以及未转化为LDL的VLDL代谢程度的调节；这两个过程可能均由载脂蛋白B/E受体介导，且似乎会随着VLDL生成增加而增强。
