INFLUENCE OF OBESITY ON THE METABOLISM OF APOLIPOPROTEIN-B IN HUMANS
INFLUENCE OF OBESITY ON THE METABOLISM OF APOLIPOPROTEIN-B IN HUMANS
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DOI：
10.1172/jci112011
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发表时间：
1985-01-01
影响因子：
15.9
通讯作者：
HOWARD, BV
中科院分区：
文献类型：
--
作者：
EGUSA, G;BELTZ, WF;HOWARD, BV
研究了9名肥胖和7名非肥胖的皮马族印度男性的极低密度脂蛋白（VLDL）、中密度脂蛋白（IDL）和低密度脂蛋白（LDL）中载脂蛋白B（apo B）代谢的影响。本文研究了注射自体B（131）I-VLDL、[~ 3 H]甘油和自体~（125）I-LDL后，VLDL-B、VLDL-TG、IDL-B和LDL-B的动力学。在从所有脂蛋白组分中分离的载脂蛋白B和从VLDL中分离的甘油三酯中测定比活性。通过多房室分析测定VLDL、IDL和LDL中载脂蛋白B的转运率和部分分解代谢率，以及VLDL中甘油三酯的转运率和部分分解代谢率。该方法还允许估计脂蛋白的相互转化率。这两组的平均年龄和身高相似，但肥胖组的总体重较高（131 ± 0.01）。14对66 +-。3公斤。SEM [平均值的标准误差]）和无脂肪质量（81 . ±. 5对54 +-。2 kg）。两组的血浆总脂质相似，肥胖和消瘦受试者中VLDL、IDL和LDL中的apo B浓度相似。尽管浓度相似，但肥胖受试者与瘦受试者相比具有更高的VLDL-甘油三酯合成率（62.6 ± 0.01）。15 vs. 26.2 .+-。7g/d，P < 0.01），VLDL-B（2241 . ±. 215对1113 +-。72 mg/d，P < 0.001），LDL-B（1234 . ±. 87对802 +-。83 mg/d，P < 0.01）。在肥胖受试者中，从循环中清除的VLDL-B量显著更高，而LDL-B没有转化（1078 . ±. 159对460 +-。34 mg/d，P < 0.05），肥胖受试者的LDL分解率分数高于瘦对照组（0.48 ± 0.05）。0.02相对于0.41 ±。0.02 d-1，P > 0.05）。在肥胖个体中，LDL的快速分解和VLDL代谢增加而不转化为LDL可能是维持LDL在正常水平的机制，尽管其前体过量产生。
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 9 obese and 7 nonbese 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 2 groups had similar mean ages and heights, but the obese group had a higher total body weight (131 .+-. 14 vs. 66 .+-. 3 kg .+-. SEM [standard error of the mean]) and fat free mass (81 .+-. 5 vs. 54 .+-. 2 kg) than lean controls. Plasma total lipids were similar for the 2 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 [day], P < 0.01), VLDL-B (2241 .+-. 215 vs. 1113 .+-. 72 mg/d, P < 0.001), and LDL-B (1234 .+-. 87 vs. 802 .+-. 83 mg/d, P < 0.01). In obese subjects, significantly higher amounts of VLDL-B were removed from the circulation without conversion of LDL-B (1078 .+-. 159 vs. 460 .+-. 34 mg/d, P < 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 > 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.