Chylomicrons are assembled in the intestinal mucosa as a means to transport dietary cholesterol and triacylglycerols to the rest of the body. Chylomicrons are, therefore, the molecules formed to mobilize dietary (exogenous) lipids. The predominant lipids of chylomicrons are triacylglycerols (see Table above). The apolipoproteins that predominate before the chylomicrons enter the circulation include apoB-48 and apoA-I, -A-II and IV. ApoB-48 combines only with chylomicrons.
Chylomicrons leave the intestine via the lymphatic system and enter the circulation at the left subclavian vein. In the bloodstream, chylomicrons acquire apoC-II and apoE from plasma HDLs. In the capillaries of adipose tissue and muscle, the fatty acids of chylomicrons are removed from the triacylglycerols by the action of lipoprotein lipase (LPL), which is found on the surface of the endothelial cells of the capillaries. The apoC-II in the chylomicrons activates LPL in the presence of phospholipid. The free fatty acids are then absorbed by the tissues and the glycerol backbone of the triacylglycerols is returned, via the blood, to the liver and kidneys. Glycerol is converted to the glycolytic intermediate dihydroxyacetone phosphate (DHAP). During the removal of fatty acids, a substantial portion of phospholipid, apoA and apoC is transferred to HDLs. The loss of apoC-II prevents LPL from further degrading the chylomicron remnants.
Chylomicron remnants, containing primarily cholesteryl esters, apoE and apoB-48, are then delivered to, and taken up by, the liver through interaction with the LDL receptor which requires apoE or via the chylomicron remnant receptor, which is a member of the LDL receptor-related protein (LRP) family. The recognition of chylomicron remnants by the hepatic remnant receptor also requires apoE. Chylomicrons function to deliver dietary triacylglycerols to adipose tissue and muscle and dietary cholesterol to the liver.
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