LDL and apoB
LDL acts as a secondary cholesteryl ester donor to chylomicrons via CETP during postprandial lipemia (Atherosclerosis 1999)
Original title: Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects
In normolipidemic subjects, apo B- and apo AI-containing lipoproteins were tracked over 8 hours following a mixed meal. Plasma apo AI fell 12% by 3 hours (P<0.005), HDL2 rose 13% by 4 hours while HDL3 fell 9% by 3 hours (both P<0.005 and P<0.05), and plasma LDL fell 5% by 3 hours (P<0.05) with a 10% reduction in its cholesteryl ester to triglyceride ratio at 2 hours (P<0.005) alongside rising LDL triglyceride content. Despite LDL's high capacity to accept cholesteryl ester from HDL via CETP, no measurable increase in LDL cholesteryl ester content was detected postprandially, and the authors show that cholesteryl ester accepted by LDL from HDL is secondarily transferred onward to chylomicrons by CETP, given chylomicrons' far lower cholesteryl ester to triglyceride ratio than LDL. The findings indicate that elevated postprandial chylomicron levels induce LDL to act as a secondary CETP-mediated cholesteryl ester donor.
Original abstract
Postprandial hypertriglyceridemia represents an independent risk factor for coronary artery disease. In the postprandial state, elevated levels of triglyceride-rich lipoproteins (TRL) are minor acceptors of HDL-cholesteryl ester (CE) transferred by CETP in normolipidemic subjects: indeed, LDL particles represent the major CE acceptors. In order to evaluate further the potential atherogenicity of lipoprotein particles characteristic of the postprandial phase in normolipidemic subjects, we determined the quantitative and qualitative features of apoB- and apoAI-containing lipoproteins over an 8-h period following consumption of a mixed meal. During postprandial lipemia, we observed a significant decrease (-12%) in plasma AI concentration (138+/-4 and 156+/-4 mg/dl, at 3 h and baseline, respectively, P<0.005). Concomitantly, a progressive increase (+13%) was detected in HDL2 concentrations (138+/-7 mg/dl at 4 h vs. 122+/-12 mg/dl at baseline, P<0.005), as well as a significant reduction (-9%) in HDL3 levels (137+/-6 mg/dl at 3 h vs. 150+/-4 mg/dl at baseline; P<0.05). Additionally, plasma LDL was reduced by 5% (247+/-12 mg/dl at 3 h vs. 260+/-15 mg/dl at baseline; P<0.05) 3 h following meal intake. Moreover, a significant reduction (-10%) occurred in the CE/TG ratio in LDL at 2 h postprandially (8+/-2 at 2 h vs. 9+/-3 at baseline; P<0.005). These changes reflected an increment (17+/-3 mg/dl at 3 h vs. 15+/-4 mg/dl at baseline; P<0.05) in LDL triglyceride concentrations. Despite the high CE acceptor capacity of LDL particles, no measurable increase in their CE content was detected during the postprandial phase. We demonstrated that CE accepted by LDL particles from HDL are secondarily transferred to chylomicrons by CETP. As chylomicrons displayed a 260-fold lower CE/TG ratio than LDL (0.03:1 and 7.8:1 in chylomicrons and LDL, respectively), CE-rich LDL may act to donate CE to chylomicrons. In conclusion, our data indicate that the presence of elevated levels of chylomicrons induces LDL to act as a secondary donor of CE during the postprandial phase.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.