HDL biology
Atorvastatin cuts postprandial CETP-mediated cholesteryl ester transfer from HDL to chylomicrons by up to 26% (J Clin Endocrinol Metab 2002)
Original title: Atorvastatin reduces postprandial accumulation and cholesteryl ester transfer protein-mediated remodeling of triglyceride-rich lipoprotein subspecies in type IIb hyperlipidemia
Researchers gave 11 subjects with type IIB hyperlipidemia atorvastatin 10 mg or 40 mg for 6 weeks to test effects on postprandial lipoprotein remodeling. Atorvastatin significantly reduced the postprandial rise in triglycerides (-42% and -55% at 10 and 40 mg, P<0.01), chylomicrons (-24% and -40%, P<0.03), and VLDL-1 (-54% and -52%, P<0.02). Before treatment, postprandial cholesteryl ester transfer from HDL to chylomicrons increased 2.5-fold (P<0.005), to VLDL-1 1.8-fold (P<0.005), to VLDL-2 1.4-fold (P<0.05), and to intermediate-density lipoproteins 1.4-fold (P<0.05) at 4 hours; after treatment, cholesteryl ester transfer from HDL to triglyceride-rich lipoproteins at 4 hours fell 26% at 10 mg and 24% at 40 mg (both P<0.05), driven specifically by reduced transfer to chylomicrons. The authors conclude atorvastatin attenuates abnormal postprandial remodeling of triglyceride-rich lipoproteins in type IIB hyperlipidemia mainly by reducing CETP-mediated cholesteryl ester transfer.
Original abstract
The effect of atorvastatin, at 10 mg or 40 mg for 6 wk, on lipid and lipoprotein metabolism during the postprandial phase in subjects (n = 11) displaying type IIB hyperlipidemia was evaluated. The postprandial increment in area under the curve above baseline concentrations in type IIB subjects was significantly decreased by atorvastatin for plasma triglyceride (A10: -42% and A40: -55%, P < 0.01), chylomicrons (CMs) (A10: -24% and A40: -40%, P < 0.03) and VLDL-1 (A10: -54% and A40: -52%, P < 0.02). Before atorvastatin therapy, postprandial cholesteryl ester (CE) transfer from high-density lipoprotein (HDL) to CMs (2.5-fold; P < 0.005), very low-density lipoprotein (VLDL)-1 (1.8-fold; P < 0.005), VLDL-2 (1.4-fold; P < 0.05), and intermediate-density lipoproteins (1.4-fold; P < 0.05) were significantly increased 4 h postprandially. Following statin treatment, the postprandial transfer of CE from HDL to triglyceride-rich lipoproteins (TRLs) at the 4-h time point was significantly reduced at 10 mg/d (-26%; P < 0.05) and at 40 mg/d (-24%; P < 0.05), compared with that before treatment. Such postprandial increase in CE transferred from HDLs to TRLs arose exclusively from accelerated CE transfer from HDLs to CMs (2.5-fold; P < 0.005). In conclusion, atorvastatin attenuates the abnormal intravascular remodeling of postprandial TRL particles via marked reduction in CE transfer in type IIB hyperlipidemia and diminishes the postprandial formation and accumulation of CMs and VLDL-1.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.