Plasma apolipoprotein changes in the triglyceride-rich lipoprotein fraction of human subjects fed a fat-rich meal.
Plasma apolipoprotein changes in the triglyceride-rich lipoprotein fraction of human subjects fed a fat-rich meal.
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喂食富含脂肪膳食的人类受试者中富含甘油三酯的脂蛋白部分的血浆载脂蛋白发生变化。
DOI：
10.1016/s0022-2275(20)38485-6
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发表时间：
1988
影响因子：
6.5
通讯作者：
E. Schaefer
中科院分区：
文献类型：
--
作者：
J. Cohn;J. Mcnamara;S. D. Cohn;J. Ordovás;E. Schaefer
22名受试者（9名男性，13名女性）被喂食富含脂肪的膳食（每公斤体重1克脂肪）。饭后0、3、6、9和12小时，用超离心法分离富甘油三酯脂蛋白（TRL） （d < 1.006 g/ml）。餐后血浆甘油三酯先升高后降低，血浆载脂蛋白a - 1和载脂蛋白b浓度降低。TRL甘油三酯、TRL总蛋白和TRL载脂蛋白浓度均在高脂餐后先升高后降低。餐后血浆甘油三酯升高与空腹血浆甘油三酯水平显著相关（r = 0.66, P < 0.001）；餐后TRL甘油三酯升高与空腹TRL甘油三酯水平显著相关（r = 0.58, P < 0.01）；然而，餐后TRL载脂蛋白升高与空腹TRL载脂蛋白水平无显著相关（r = 0.37， N.S.）。用聚丙烯酰胺梯度（4-22.5%）凝胶电泳分离TRL载脂蛋白，用激光密度计对蛋白质条带进行二维扫描。测定餐后TRL载脂蛋白浓度的相对变化。TRL apoB-100、apoB-48、apoE和apoC在餐后先升高后降低。通过单克隆抗体ELISA法直接测定8例受试者的apoB-100，证实富脂餐后TRL apoB-100升高。TRL中ApoA-I的浓度没有变化。餐后12小时，TRL部分中的白蛋白显著增加。餐后甘油三酯血症严重的受试者TRL甘油三酯和TRL载脂蛋白ob的升高幅度较大，但其TRL载脂蛋白ob -100/载脂蛋白ob -48比值与甘油三酯血症不明显的受试者没有差异。假设含有载脂蛋白b -100的血浆TRL主要来自肝脏，我们的数据表明，肝脏和肠道富含甘油三酯的脂蛋白对餐后甘油三酯血症有重要贡献。
Twenty two subjects (9 males, 13 females) were fed a fat-rich meal (1 g of fat/kg body weight). Triglyceride-rich lipoproteins (TRL) were isolated by ultracentrifugation (d less than 1.006 g/ml) from blood drawn 0, 3, 6, 9, and 12 hr after the meal. Plasma triglyceride increased then decreased postprandially, while plasma apoA-I and apoB concentrations decreased. TRL triglyceride, TRL total protein, and TRL apoB concentrations all increased then decreased after the fat-rich meal. Postprandial rise in plasma triglyceride was significantly correlated with fasting plasma triglyceride levels (r = 0.66, P less than 0.001); postprandial rise in TRL triglyceride was significantly correlated with fasting TRL triglyceride levels (r = 0.58, P less than 0.01); postprandial rise in TRL apoB was not, however, significantly correlated with fasting TRL apoB levels (r = 0.37, N.S.). TRL apolipoproteins were separated by polyacrylamide gradient (4-22.5%) gel electrophoresis and protein bands were scanned in two dimensions with a laser densitometer. Relative postprandial changes in the concentration of the TRL apolipoproteins were determined. TRL apoB-100, apoB-48, apoE, and apoC increased then decreased postprandially. The increase in TRL apoB-100 after the fat-rich meal was confirmed in 8 subjects by direct measurement of apoB-100 with a monoclonal antibody ELISA assay. ApoA-I concentration in TRL was unchanged. Albumin in the TRL fraction was significantly increased 12 hr after the meal. Subjects with a greater magnitude of postprandial triglyceridemia had a greater increase in TRL triglyceride and TRL apoB, but their TRL apoB-100/apoB-48 ratios were not different from subjects with less pronounced triglyceridemia. Assuming that plasma TRL containing apoB-100 are predominantly derived from the liver, our data suggest that triglyceride-rich lipoproteins from both the liver and intestine make a significant contribution to postprandial triglyceridemia.
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