Abstract
: Oxidized low density lipoprotein (Ox-LDL) and chylomicron (CM) remnants were proposed previously as the most atherogenic lipoproteins which initiate and progress the coronary atherosclerosis as the causal lipoproteins. However, there are still controversies on these hypothesizes. Therefore, we propose a new hypothesis on postprandial remnant lipoproteins (RLP) which contain hepatic origin apoB100 and intestinal origin apoB48 in VLDL fraction. Plasma RLP-cholesterol (RLP-C) and RLP-triglyceride (RLP-TG) increased significantly after fat load associated with the increase of TG. Approximately above 80% of the increased TG after fat load is composed of TG in RLP. Postprandial RLP contained significantly greater apoB100 lipoprotein particles than apoB48 particles. Also most LPL in non-heparin plasma was found in RLP as RLP-LPL complex and found in circulation and incorporated in peripheral issues primarily for energy delivery as a ligand for VLDL receptor. Plasma LPL concentration and activity don’t increase in plasma after fat intake, therefore it may cause the insufficient hydrolysis of RLP. As the results, we observed the significant increase of RLP-TG concentration with large particle size as mostly VLDL remnants in postprandial plasma. Therefore, LPL concentration was inversely correlated with RLP-C and RLP-TG concentration in postprandial plasma. Increased postprandial TG associated with increased RLP having striking similarity with Ox-LDL has been shown as the risk of cardiovascular disease by large epidemiological studies. We have shown that VLDL remnants, not CM remnants, are the major atherogenic lipoproteins increased in postprandial plasma associated with insufficient LPL activity as the possible causal factor for the initiation of atherosclerosis. Therefore, overproduced RLP in postprandial plasma should be the initial target to be controlled as the initiator of atherosclerosis by choosing the kind of food intake and appropriate exercise, without using therapeutic drugs.
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