Egusa G, Beltz W F, Grundy S M, Howard B V
J Clin Invest. 1985 Aug;76(2):596-603. doi: 10.1172/JCI112011.
The influence of obesity on the metabolism of apolipoprotein B (apo B) in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) was investigated in nine obese and seven nonobese Pima Indian men. Kinetics of VLDL-apo B (VLDL-B), VLDL-triglycerides, IDL-B and LDL-B were studied after injection of autologous 131I-VLDL, [3H]glycerol, and autologous 125I-LDL. Specific activities were measured in apo B isolated from all lipoprotein fractions and in triglyceride isolated from VLDL. Transport rates and fractional catabolic rates for apo B in VLDL, IDL, and LDL and triglyceride in VLDL were determined by multicompartmental analysis. This method also allowed the estimation of rates of interconversions of the lipoproteins. The two groups had similar mean ages and heights, but the obese group had a higher total body weight (131 +/- 14 vs. 66 +/- 3 kg +/- SEM) and fat free mass (81 +/- 5 vs. 54 +/- 2 kg) than lean controls. Plasma total lipids were similar for the two groups, and apo B concentrations in VLDL, IDL, and LDL were similar in obese and lean subjects. In spite of similarity in concentrations, obese subjects compared to lean subjects had higher synthetic rates of VLDL-triglyceride (62.6 +/- 15 vs. 26.2 +/- 7 g/d, P less than 0.01), VLDL-B (2,241 +/- 215 vs. 1,113 +/- 72 mg/d, P less than 0.001), and LDL-B (1,234 +/- 87 vs. 802 +/- 83 mg/d, P less than 0.01). Furthermore, in obese subjects, significantly higher amounts of VLDL-B were removed from the circulation without conversion to LDL-B (1,078 +/- 159 vs. 460 +/- 34 mg/d, P less than 0.05), and obese subjects had a higher fractional catabolic rate for LDL than the lean controls (0.48 +/- 0.02 vs. 0.41 +/- 0.02 d-1, P less than 0.05). The rapid catabolism of LDL and increased metabolism of VLDL without conversion to LDL in obese individuals may be mechanisms for maintenance of LDL at normal levels despite the overproduction of its precursor.
在9名肥胖的皮马印第安男性和7名非肥胖的皮马印第安男性中，研究了肥胖对极低密度脂蛋白（VLDL）、中间密度脂蛋白（IDL）和低密度脂蛋白（LDL）中载脂蛋白B（apo B）代谢的影响。注射自体131I-VLDL、[3H]甘油和自体125I-LDL后，研究了VLDL-apo B（VLDL-B）、VLDL-甘油三酯、IDL-B和LDL-B的动力学。测量了从所有脂蛋白组分中分离出的apo B以及从VLDL中分离出的甘油三酯的比活性。通过多室分析确定了VLDL、IDL和LDL中apo B以及VLDL中甘油三酯的转运速率和分解代谢率。该方法还可以估计脂蛋白的相互转化速率。两组的平均年龄和身高相似，但肥胖组的总体重（131±14 vs. 66±3 kg±SEM）和去脂体重（81±5 vs. 54±2 kg）高于瘦对照组。两组的血浆总脂质相似，肥胖和瘦受试者的VLDL、IDL和LDL中的apo B浓度也相似。尽管浓度相似，但与瘦受试者相比，肥胖受试者的VLDL-甘油三酯合成速率更高（62.6±15 vs. 26.2±7 g/d，P<0.01），VLDL-B合成速率更高（2241±215 vs. 1113±72 mg/d，P<0.001），LDL-B合成速率更高（1234±87 vs. 802±83 mg/d，P<0.01）。此外，在肥胖受试者中，从循环中清除的未转化为LDL-B的VLDL-B量显著更高（1078±159 vs. 460±34 mg/d，P<0.05），肥胖受试者的LDL分解代谢率高于瘦对照组（0.48±0.02 vs. 0.41±0.02 d-1，P<0.05）。肥胖个体中LDL的快速分解代谢以及VLDL在未转化为LDL的情况下代谢增加，可能是尽管其前体过量产生但仍将LDL维持在正常水平的机制。
