Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression?
Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression?
复制标题
DOI：
10.1152/ajpendo.2001.281.3.e626
复制
发表时间：
2001-09-01
影响因子：
5.1
通讯作者：
Pal, S
中科院分区：
文献类型：
--
作者：
Mamo, JCL;Watts, GF;Pal, S
研究人员在内脏肥胖的中年男性中研究了口服脂肪挑战后的餐后血脂。两组的血浆胆固醇水平相似，但肥胖受试者的血浆甘油三酯水平较高，高密度胆固醇含量减少。由于伴随胰岛素抵抗，肥胖受试者的空腹血浆胰岛素高出四倍，计算出的 HOMA 评分分别为 3.1 +/- 0.6 和 0.8 +/- 0.2。口服脂肪挑战后，血浆载脂蛋白 B-48 (apoB(48)) 和视黄醇棕榈酸酯 (RP) 用于监测乳糜微粒代谢。与瘦人相比，肥胖者的 apoB48 空腹浓度高出两倍多，这表明水解后颗粒的积累。口服脂质负荷后，肥胖受试者的apoB（48）和RP曲线下增量面积（IAUC）均显着更大（apoB48：分别为97 +/- 17 vs. 44 +/- 12 mug.ml(-1).h；RP：3,120 +/- 511 vs. 1,308 +/- 177 U.ml(-1).h）。乳糜微粒转化为残余物的延迟可能导致内脏肥胖受试者的餐后血脂异常。肥胖受试者的甘油三酯 IAUC 高出 68%（4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM.h，P < 0.06）。此外，肥胖受试者的餐后甘油三酯峰值延迟了 2 小时。体内甘油三酯脂解的减少似乎并不反映水解酶活性的变化。发现瘦和肥胖受试者的肝素后血浆脂肪酶率相似。在这项研究中，单核细胞上的低密度脂蛋白（LDL）受体表达被用作肝活动的替代标志物。我们发现，在肥胖受试者中，与瘦对照相比，LDL 结合减少了一半（70.9 +/- 15.07 vs. 38.9 +/- 4.6 ng LDL 结合/mug 细胞蛋白，P = 0.02）。由于 LDL 受体参与清除促动脉粥样硬化的乳糜微粒残余物，因此我们认为，在胰岛素抵抗的肥胖受试者中，这些颗粒的肝脏清除可能会受到损害。内脏肥胖、胰岛素抵抗受试者过早和加速的动脉粥样硬化形成可能部分反映了餐后脂蛋白残余物的清除延迟。
Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 +/- 0.6 vs. 0.8 +/- 0.2, respectively. Plasma apolipoprotein B-48 (apoB(48)) and retinyl palmitate (RP) after an oral fat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB48 was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB(48) and RP curves (IAUC) were both significantly greater in obese subjects (apoB48: 97 +/- 17 vs. 44 +/- 12 mug.ml(-1).h; RP: 3,120 +/- 511 vs. 1,308 +/- 177 U.ml(-1).h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM.h, P < 0.06). Moreover, peak postprandial triglyceride was delayed by 2 h in obese subjects. The reduction in triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to be similar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on mononuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 +/- 15.07 vs. 38.9 +/- 4.6 ng LDL bound/mug cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, we suggest that the hepatic clearance of these particles might be compromised in insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.