Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. Remnant lipoproteins become attached to the vascular wall, where they can penetrate intact endothelium causing foam cell formation. Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate the expression of endothelial adhesion molecules, facilitate adhesion and migration of inflammatory cells into the subendothelial space, and activate the complement system. Since humans are postprandial most of the day, the continuous generation of remnants after each meal may be one of the triggers for the development of atherosclerosis. Modulation of postprandial lipemia by lifestyle changes and pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options. 1. Introduction Atherosclerosis is the primary cause of death in the world [1]. Classical risk factors such as smoking, hypertension, fasting hyperlipidemia, insulin resistance, increased body fat mass, and unfavourable body fat distribution are strongly interrelated and can often be found in one and the same subject. Subjects with fasting hypertriglyceridemia usually have elevated postprandial lipids due to the close correlation of fasting and postprandial triglycerides (TG) [2]. Postprandial lipemia has gained interest because of recent reports showing that nonfasting TG independently predict the risk for atherosclerosis [3, 4] and are possibly even stronger predictors of cardiovascular disease (CVD) than fasting TG [3, 5]. Atherosclerosis is considered a low-grade chronic inflammatory disease [6], and both the postprandial phase and chronic disease states such as the metabolic syndrome are associated with increased inflammation. This paper outlines recent developments in the understanding of postprandial inflammation and its relationship with vascular function, metabolic diseases, and lifestyle behaviour. 2. Metabolism of Postprandial Lipemia Dietary fat is absorbed in the intestine and secreted into lymph by enterocytes in TG-rich chylomicrons. Once in the circulation, chylomicrons rapidly undergo hydrolysis to produce cholesterol-dense lipoprotein remnants which are taken up by the liver [7, 8]. After a fatty meal,
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