PREFERENTIAL CHOLESTERYL ESTER ACCEPTORS AMONG TRIGLYCERIDE-RICH LIPOPROTEINS DURING ALIMENTARY LIPEMIA IN NORMOLIPIDEMIC SUBJECTS

Triglyceride-rich lipoproteins (TRLs), namely chylomicrons (CMs), VLDL , and their remnants, are implicated in the atherogenic features of po stprandial lipemia. In human plasma, cholesteryl ester transfer protei n (CETP) mediates the heteroexchange of neutral lipids, ie, triglyceri des (TG) and cholesteryl esters (CE), between distinct subpopulations of apoB- and of apoAI-containing lipoproteins. In fasting normolipidem ic plasma, CETP plays an antiatherogenic role by promoting preferentia l CE redistribution from HDL to LDL particles of intermediate subclass with optimal binding affinity for the cellular LDL receptor. While th e relative proportions and chemical compositions of donor and acceptor lipoproteins are known to influence CETP activity, elevated levels of TRL present during alimentary lipemia have been proposed to be associ ated with enhanced CETP activity. To identify the preferential CE acce ptor particles among postprandial TRL subfractions, we investigated th e effects of a typical Western meal (1200 kcal, 14% protein; 38% carbo hydrate; and 48% fat, monounsaturated/polyunsaturated ratio 4:1) on th e rates of postprandial CE transfer from HDL to apoB-containing lipopr oteins in normolipidemic subjects (n=13). Two hours postprandially, pl asma levels of TRL were significantly elevated (140 versus 51 mg/dL at baseline, P=.0001). Total rates of CE transferred (88+/-7 mu g.h(-1). mL(-1)) from HDL to apoB-containing lipoproteins were not significantl y modified by alimentary lipemia over a period of 8 hours. Quantitativ ely, LDL accepted 64+/-5 mu g CE per hour per milliliter plasma from H DL, whereas CM (Sf>400), VLDL1 (Sf 60 to 400), VLDL2 (Sf 20 to 60), an d IDL (Sf 12 to 20) accepted 5+/-3, 16+/-3, 1.4+/-0.3, and 1.5+/-0.2, respectively. Quantitatively, VLDL1 was the major CE acceptor among TR Ls (P=.0001); thus, VLDL1, but not CMs, represented the major CE accep tor among TRLs. Qualitatively however, VLDL2 and IDL displayed a highe r capacity to accept CE from HDL (51.6+/-4.1 and 46.3+/-2.8 mu g CE tr ansferred per hour per milligram lipoprotein, respectively; P<.005) co mpared with CM, VLDL1, and LDL (12.6+/-2.8, 34.7+/-4.2, and 22.7+/-2.0 mu g CE transferred per hour per milligram lipoprotein, respectively) . In conclusion, elevated postprandial TRL, levels are not associated with enhanced total CE transfer to these particles. Furthermore, the q ualitative features of postprandial CE transfer from HDL to CM and VLD L1 were not related to the relative TG content of these particles. The CETP-facilitated enrichment of VLDL1 in CE therefore identifies them as potentially atherogenic particles during the postprandial phase.