Lewis G F, O'Meara N M, Soltys P A, Blackman J D, Iverius P H, Druetzler A F, Getz G S, Polonsky K S
Department of Medicine, University of Chicago, Pritzker School of Medicine, Illinois 60637.
J Clin Endocrinol Metab. 1990 Oct;71(4):1041-50. doi: 10.1210/jcem-71-4-1041.
Abnormalities in fasting lipid and lipoprotein levels are known to occur in obesity and other hyperinsulinemic states. However, postprandial lipoprotein metabolism has not been studied systematically in obese subjects using sensitive techniques to distinguish between triglyceride-rich lipoprotein particles derived from the intestine and the liver. In the present study the vitamin A fat-loading test was used to label intestinally derived triglyceride-rich lipoprotein particles in the postprandial state. Lipid parameters in seven normolipidemic obese subjects [body mass index, 43.7 +/- 2.81 kg/m2 (mean +/- SEM)] were compared to those in eight matched normal weight controls (body mass index, 23.6 +/- 0.72 kg/m2) during the 24-h period following ingestion of a mixed meal with a high fat content to which vitamin A had been added. Although subjects were selected for normal fasting lipid levels, in the obese group fasting triglycerides were significantly higher (1.35 +/- 0.12 vs. 0.68 +/- 0.08 mmol/L; P less than 0.0005) and high density lipoprotein (HDL) cholesterol was lower (0.94 +/- 0.08 vs. 1.35 +/- 0.11 mmol/L; P less than 0.01). The obese subjects had a greater postprandial triglyceride response to the test meal (P less than 0.05). The cumulative increment in total plasma triglycerides was 3.35-fold greater in obese than control subjects, while that of retinyl ester was only 1.63-fold greater, suggesting that a significant portion of the postprandial triglyceride response is due to endogenous hepatic lipoproteins. Postprandial plasma triglyceride and retinyl ester increment correlated with basal triglycerides (r = 0.72; P less than 0.005 and r = 0.57; P less than 0.03, respectively) and negatively with fasting HDL (r = -0.51; P less than 0.05 and r = -0.60; P less than 0.02, respectively). In the obese, the HDL triglyceride content increased maximally 4 h postprandially (4.1% to 6.1%; P less than 0.005) and phospholipid at 12 h (25.8% to 28.7%; P less than 0.05), with lower cholesteryl ester (21.1% to 17.5%; P less than 0.002) at 8 h, reflecting exchange of surface and core lipids with triglyceride-rich particles after the meal. In obese and control subjects the magnitude of HDL triglyceride enrichment after the meal correlated positively with the postprandial triglyceride increment (r = 0.74; P less than 0.007) and negatively with the fasting HDL cholesterol concentration (r = -0.80; P = 0.002). We conclude that even normolipidemic obese subjects have greater postprandial lipemia and triglyceride enrichment of HDL after ingestion of a high fat meal.(ABSTRACT TRUNCATED AT 400 WORDS)
已知肥胖症和其他高胰岛素血症状态会出现空腹血脂和脂蛋白水平异常。然而，尚未采用敏感技术对肥胖受试者的餐后脂蛋白代谢进行系统研究，以区分源自肠道和肝脏的富含甘油三酯的脂蛋白颗粒。在本研究中，维生素A脂肪负荷试验用于标记餐后状态下源自肠道的富含甘油三酯的脂蛋白颗粒。在摄入添加了维生素A的高脂肪混合餐后的24小时内，将7名血脂正常的肥胖受试者[体重指数，43.7±2.81kg/m²（平均值±标准误）]的血脂参数与8名匹配的正常体重对照者（体重指数，23.6±0.72kg/m²）的血脂参数进行比较。尽管受试者的空腹血脂水平正常，但肥胖组的空腹甘油三酯显著更高（1.35±0.12 vs. 0.68±0.08mmol/L；P＜0.0005），高密度脂蛋白（HDL）胆固醇更低（0.94±0.08 vs. 1.35±0.11mmol/L；P＜0.01）。肥胖受试者对试验餐的餐后甘油三酯反应更大（P＜0.05）。肥胖受试者血浆总甘油三酯的累积增量比对照受试者大3.35倍，而视黄酯的累积增量仅大1.63倍，这表明餐后甘油三酯反应的很大一部分归因于内源性肝脏脂蛋白。餐后血浆甘油三酯和视黄酯增量与基础甘油三酯呈正相关（r = 0.72；P＜0.005和r = 0.57；P＜0.03），与空腹HDL呈负相关（r = -0.51；P＜0.05和r = -0.60；P＜0.02）。在肥胖者中，HDL甘油三酯含量在餐后4小时最大增加（4.1%至6.1%；P＜0.005），磷脂在12小时增加（25.8%至28.7%；P＜0.05），胆固醇酯在8小时降低（21.1%至17.5%；P＜0.002），反映了餐后表面和核心脂质与富含甘油三酯颗粒的交换。在肥胖和对照受试者中，餐后HDL甘油三酯富集程度与餐后甘油三酯增量呈正相关（r = 0.74；P＜0.007），与空腹HDL胆固醇浓度呈负相关（r = -0.80；P = 0.002）。我们得出结论，即使是血脂正常的肥胖受试者，在摄入高脂肪餐后也会有更大的餐后血脂过多和HDL甘油三酯富集。（摘要截短至400字）
