Lassel T S, Guerin M, Auboiron S, Guy-Grand B, Chapman M J
Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 321 'Lipoprotéines et Athérogénèse', Hôpital de la Pitié, Pavillon Benjamin Delessert, 83 Blvd de l'Hopital, 75651, Paris, France.
Atherosclerosis. 1999 Nov 1;147(1):41-8. doi: 10.1016/s0021-9150(99)00161-6.
Postprandial hypertriglyceridemia represents an independent risk factor for coronary artery disease. In the postprandial state, elevated levels of triglyceride-rich lipoproteins (TRL) are minor acceptors of HDL-cholesteryl ester (CE) transferred by CETP in normolipidemic subjects: indeed, LDL particles represent the major CE acceptors. In order to evaluate further the potential atherogenicity of lipoprotein particles characteristic of the postprandial phase in normolipidemic subjects, we determined the quantitative and qualitative features of apoB- and apoAI-containing lipoproteins over an 8-h period following consumption of a mixed meal. During postprandial lipemia, we observed a significant decrease (-12%) in plasma AI concentration (138+/-4 and 156+/-4 mg/dl, at 3 h and baseline, respectively, P<0.005). Concomitantly, a progressive increase (+13%) was detected in HDL2 concentrations (138+/-7 mg/dl at 4 h vs. 122+/-12 mg/dl at baseline, P<0.005), as well as a significant reduction (-9%) in HDL3 levels (137+/-6 mg/dl at 3 h vs. 150+/-4 mg/dl at baseline; P<0.05). Additionally, plasma LDL was reduced by 5% (247+/-12 mg/dl at 3 h vs. 260+/-15 mg/dl at baseline; P<0.05) 3 h following meal intake. Moreover, a significant reduction (-10%) occurred in the CE/TG ratio in LDL at 2 h postprandially (8+/-2 at 2 h vs. 9+/-3 at baseline; P<0.005). These changes reflected an increment (17+/-3 mg/dl at 3 h vs. 15+/-4 mg/dl at baseline; P<0.05) in LDL triglyceride concentrations. Despite the high CE acceptor capacity of LDL particles, no measurable increase in their CE content was detected during the postprandial phase. We demonstrated that CE accepted by LDL particles from HDL are secondarily transferred to chylomicrons by CETP. As chylomicrons displayed a 260-fold lower CE/TG ratio than LDL (0.03:1 and 7.8:1 in chylomicrons and LDL, respectively), CE-rich LDL may act to donate CE to chylomicrons. In conclusion, our data indicate that the presence of elevated levels of chylomicrons induces LDL to act as a secondary donor of CE during the postprandial phase.
餐后高甘油三酯血症是冠状动脉疾病的独立危险因素。在餐后状态下,富含甘油三酯的脂蛋白(TRL)水平升高,在血脂正常的受试者中,它们是胆固醇酯转移蛋白(CETP)转移的高密度脂蛋白胆固醇酯(CE)的次要受体:实际上,低密度脂蛋白颗粒是主要的CE受体。为了进一步评估血脂正常受试者餐后阶段脂蛋白颗粒的潜在致动脉粥样硬化性,我们在进食混合餐后8小时内测定了含载脂蛋白B和载脂蛋白AI的脂蛋白的定量和定性特征。在餐后血脂升高期间,我们观察到血浆载脂蛋白AI浓度显著下降(-12%)(分别在3小时和基线时为138±4和156±4mg/dl,P<0.005)。同时,检测到高密度脂蛋白2浓度逐渐升高(+13%)(4小时时为138±7mg/dl,基线时为122±12mg/dl,P<0.005),以及高密度脂蛋白3水平显著降低(-9%)(3小时时为137±6mg/dl,基线时为150±4mg/dl;P<0.05)。此外,进食后3小时血浆低密度脂蛋白降低了5%(3小时时为247±12mg/dl,基线时为260±15mg/dl;P<0.05)。此外,餐后2小时低密度脂蛋白中的CE/TG比值显著降低(-10%)(2小时时为8±2,基线时为9±3;P<0.005)。这些变化反映了低密度脂蛋白甘油三酯浓度的增加(3小时时为17±3mg/dl,基线时为15±4mg/dl;P<0.05)。尽管低密度脂蛋白颗粒具有较高的CE受体能力,但在餐后阶段未检测到其CE含量有可测量的增加。我们证明,低密度脂蛋白颗粒从高密度脂蛋白接受的CE随后被CETP转移到乳糜微粒。由于乳糜微粒的CE/TG比值比低密度脂蛋白低260倍(乳糜微粒和低密度脂蛋白中分别为0.03:1和7.8:1),富含CE的低密度脂蛋白可能会将CE捐赠给乳糜微粒。总之,我们的数据表明,乳糜微粒水平升高会导致低密度脂蛋白在餐后阶段充当CE的次要供体。