Alipour A, Elte J W F, van Zaanen H C T, Rietveld A P, Cabezas M Castro
Department of Internal Medicine, St Franciscus Gasthuis, Center for Diabetes and Vascular Medicine, PO Box 10900, 3004 BA Rotterdam, The Netherlands.
Biochem Soc Trans. 2007 Jun;35(Pt 3):466-9. doi: 10.1042/BST0350466.
Postprandial hyperlipidaemia is a common metabolic disturbance in atherosclerosis. During the postprandial phase, chylomicrons and their remnants can penetrate the intact endothelium and cause foam cell formation. These particles are highly atherogenic after modification. People in the Western world are non-fasting for most of the day, which consequently leads to a continuous challenge of the endothelium by atherogenic lipoproteins and their remnants. Furthermore, atherosclerosis is considered a low-grade chronic inflammatory disease. Many studies have shown that the process of atherogenesis in part starts with the interaction between the activated leucocytes and activated endothelium. Postprandial lipoproteins can activate leucocytes in the blood and up-regulate the expression of leucocyte adhesion molecules on the endothelium, facilitating adhesion and migration of inflammatory cells into the subendothelial space. Another inflammatory process associated with postprandial lipaemia is the activation of the complement system. Its central component C3 has been associated with obesity, coronary sclerosis, the metabolic syndrome and fasting and postprandial TAGs (triacylglycerols). Moreover, chylomicrons are the strongest stimulators of adipocyte C3 production via activation of the alternative complement cascade. A postprandial C3 increment has been shown in healthy subjects and in patients with CAD (coronary artery disease) and with FCHL (familial combined hyperlipidaemia). Postprandial lipaemia has been related to TAG and free fatty acid metabolism. All of these mechanisms provide an alternative explanation for the atherogenicity of the postprandial period.
餐后高脂血症是动脉粥样硬化中常见的代谢紊乱。在餐后阶段，乳糜微粒及其残粒可穿透完整的内皮并导致泡沫细胞形成。这些颗粒在修饰后具有高度致动脉粥样硬化性。西方世界的人们一天中大部分时间都处于非空腹状态，这导致致动脉粥样硬化脂蛋白及其残粒持续对内皮造成挑战。此外，动脉粥样硬化被认为是一种低度慢性炎症性疾病。许多研究表明，动脉粥样硬化的过程部分始于活化的白细胞与活化的内皮之间的相互作用。餐后脂蛋白可激活血液中的白细胞，并上调内皮上白细胞黏附分子的表达，促进炎症细胞黏附和迁移至内皮下间隙。另一个与餐后血脂异常相关的炎症过程是补体系统的激活。其核心成分C3与肥胖、冠状动脉硬化、代谢综合征以及空腹和餐后甘油三酯有关。此外，乳糜微粒是通过激活替代补体级联反应刺激脂肪细胞产生C3的最强刺激物。在健康受试者、冠心病患者和家族性混合型高脂血症患者中均已显示出餐后C3升高。餐后血脂异常与甘油三酯和游离脂肪酸代谢有关。所有这些机制为餐后阶段的致动脉粥样硬化性提供了另一种解释。
