ROLE OF TRIGLYCERIDE-RICH LIPOPROTEINS FROM THE LIVER AND INTESTINE IN THE ETIOLOGY OF POSTPRANDIAL PEAKS IN PLASMA TRIGLYCERIDE CONCENTRATION
ROLE OF TRIGLYCERIDE-RICH LIPOPROTEINS FROM THE LIVER AND INTESTINE IN THE ETIOLOGY OF POSTPRANDIAL PEAKS IN PLASMA TRIGLYCERIDE CONCENTRATION
复制标题
DOI：
10.1016/0026-0495(89)90203-5
复制
发表时间：
1989-05-01
影响因子：
9.8
通讯作者：
SCHAEFER, EJ
中科院分区：
文献类型：
--
作者：
COHN, JS;MCNAMARA, JR;SCHAEFER, EJ
人类受试者的血浆甘油三酯浓度在摄入富含脂肪的膳食后的 12 小时内会出现一次、两次或三次峰值。含有载脂蛋白 (apo)B-48（肠道来源）的富含甘油三酯的脂蛋白 (TRL) 和含有 apoB-100（主要来自肝脏）的 TRL 均会导致餐后血浆甘油三酯浓度的变化。为了验证餐后甘油三酯血症的早期峰值主要是由于肠道分泌 TRL 所致，而较晚的峰值是由于肝脏分泌 TRL 所致的假设，在喂食富含脂肪膳食（1 g 脂肪/公斤体重）的受试者的血浆样本中测量了 TRL apoB-48、TRL apoB-100 和视黄酯（一种标记物和肠道脂蛋白）。来自 7 名受试者的数据（其中 4 名受试者喂食 40 视黄醇当量维生素 A/kg 体重，3 名受试者与脂肪餐一起喂食 20 视黄醇当量维生素 A/kg 体重），表明餐后血浆甘油三酯的峰值始终与血浆视黄酯浓度的增加相关。在四名受试者中，由于他们有两个明显的餐后甘油三酯峰值而被选中，TRL 甘油三酯、apoB-48、apoE 和 apoC 的血浆浓度随着血浆甘油三酯的较早（三小时）和较晚（九小时）峰值的增加而增加。 TRL 和 apoB-100 的增加与四名受试者中两名的两个峰值相关。我们的数据表明，1) 来自肝脏和肠道的 TRL 导致餐后甘油三酯血症的早期和晚期峰值； 2）膳食脂肪吸收后，TRL 从肠道出现的速率并不恒定。
Plasma triglyceride concentration in human subjects peaks once, twice or three times in the twelve-hour period following the ingestion of a fat-rich meal. Triglyceride-rich lipoproteins (TRL) containing apolipoprotein (apo)B-48 (of intestinal origin), and TRL containing apoB-100 (predominantly of hepatic origin) both contribute to postprandial changes in plasma triglyceride concentration. To test the hypothesis that earlier peaks in postprandial triglyceridemia are due predominantly to the secretion of TRL from the intestine, while later peaks are due to the secretion of TRL from the liver, TRL apoB-48, TRL apoB-100 and retinyl ester (a marker and intestinal lipoproteins) were measured in plasma samples from subjects fed a fat-rich meal (1 g fat/kg body wt). Data from seven subjects (four fed 40 retinol equivalents vitamin A/kg body wt. three fed 20 retinol equivalents vitamin A/kg body wt. with the fat meal), showed that postprandial peaks in plasma triglyceride were always associated with increases in plasma retinyl ester concentration. In four subjects, who were selected because they had two clearly postprandial triglyceride peaks, the plasma concentration of TRL triglyceride, apoB-48, apoE an apoC increased in conjunction with both the earlier (three hour) and later (nine hour) peaks in plasma triglyceride. Increase in TRL and apoB-100 was associated with both peaks in two of the four subjects. Our data suggest that 1) TRL from the liver and intestine contribute to both earlier and later peaks in postprandial triglyceridemia; and 2) the rate of appearance of TRL from the intestine is not constant after dietary fat absorption.