+44-7897-074717The role of nonfasting triglycerides, carried in VLDL and chylomicrons, as an independent risk factor for cardiovascular disease and death, has recently been convincingly demonstrated by evidence from prospective epidemiological large-scale studies. The accumulation of apoB-48-containing triglyceride-rich lipoproteins (TRLs) and the overproduction of large VLDL1 by the liver both occur prior to overt hyperglycemia, emphasizing the role of insulin resistance as an early pathogenic defect. The liver, adipose tissue, muscle, intestine and multiple insulin action site all exhibit insulin resistance. Together, these insulin action disruptions cause an excess of atherogenic VLDL and chylomicron remnant particles to be produced. Therefore, excessive cholesterol influx exposes the vascular wall endothelium, leading to endothelial dysfunction, oxidative stress, and prothrombotic condition over the course of the following meals. This overview reviews recent data on TRL secretion, intravascular processing, and removal accumulated over the past ten years and summarises current knowledge of diabetic postprandial dysmetabolism. Future possibilities and various therapeutic approaches are also covered. Keywords
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