POSTPRANDIAL METABOLISM OF LIPIDS AND LIP OPROTEINS

After a first partial gastric digestion, dietary fats are lipolyzed in the gut mainly by pancreatic lipase cooperation with its cofactor, co lipase. In the enterocyte, fatty acids ore reesterified, associated wi th a molecule of apolipoprotein B48, packed with phospholipids and sec reted into the lymphatic system as chylomicrons, together with apo Al, the main structural apoprotein of high density lipoprotein (HDL). In the main circulation, TG are hydrolyzed by lipoprotein lipase (LPL) at tached to capillary walls mainly of muscle where FA are oxidized and o f adipose tissue where they are stored. Chylomicrons loose apo Al and phospholipids to HLD, and acquire from them regulatory apoproteins: ap o al, the cofactor of IPL, and apo CIII which prevents premature clear ance are progressively returned to HDL, while apoE is the ligand for u ptake of chylomicron remnants by specific cellular receptors. Chylomic rons do not enter the apoB100-LDL pool which derives solely from endog enous VLDL particles. The influx of fatty acids, particularly saturate d, stimulates cholesterol synthesis and decreases the uptake of choles terol-rich low density lipoproteins (LDL) which explains the rise in c holesterol induced by high fat diets. In normal subjects, however, whe n LDL clearance is efficient, chylomicron contribution to HID postpran dially increases clearance of cell cholesterol by HDL (reverse cholest erol transport), a key mechanism in the prevention of atherosclerosis. When lipolysis is slowed down the contribution to HLD, is reduced red ucing reverse cholesterol transport Moreover chylomicrons then exchang e their TG for cholesteryl esters from HLD and become highly atherogen ic.