Burdge Graham C, Calder Philip C
Institute of Human Nutrition, Developmental Origins of Adult Health and Disease Division, Biomedical Sciences Building, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK.
Br J Nutr. 2005 Jan;93(1):3-9. doi: 10.1079/bjn20041282.
Chronic inflammation of the vascular endothelium produces endothelial dysfunction and ultimately atherogenesis. Postprandial hyperlipidaemia is an independent risk factor for cardiovascular disease. Recent studies show that the magnitude of postprandial lipaemia following a single fatty meal is negatively related to vascular function. This is associated with a transient increase in the concentrations of pro-inflammatory cytokines and soluble adhesion molecules and in pro-oxidant activity. One possible interpretation is that repeated exposure of the blood vessel wall to the activities of pro-inflammatory cytokines and pro-oxidants may damage the vascular endothelium and promote atherogenesis. Based on these results, we propose a model of a causal mechanism to explain how consumption of a fatty meal may impair vascular dysfunction.
血管内皮的慢性炎症会导致内皮功能障碍并最终引发动脉粥样硬化。餐后高脂血症是心血管疾病的独立危险因素。最近的研究表明,单次高脂餐后的餐后血脂水平与血管功能呈负相关。这与促炎细胞因子、可溶性黏附分子浓度以及促氧化活性的短暂升高有关。一种可能的解释是,血管壁反复暴露于促炎细胞因子和促氧化剂的活性中可能会损害血管内皮并促进动脉粥样硬化的发生。基于这些结果,我们提出了一个因果机制模型,以解释食用高脂餐如何损害血管功能障碍。