HDL biology
Rosuvastatin cuts CETP mass 33-37% and, in hypertriglyceridemic patients, transfer activity by 59% (Atherosclerosis 2003)
Original title: Phenotype-dependent and -independent actions of rosuvastatin on atherogenic lipoprotein subfractions in hyperlipidaemia
In a randomized, double-blind, placebo-controlled crossover trial, rosuvastatin 40 mg/day for 8 weeks was tested in normotriglyceridemic (NTG, n=13) and hypertriglyceridemic (HTG, n=16) subjects. LDL-cholesterol, apoB, IDL, and LDL circulating mass fell similarly in both groups (all P<0.001), a phenotype-independent effect, while small dense LDL, VLDL1, and remnant-like particle cholesterol fell significantly only in the HTG group. Rosuvastatin reduced CETP mass by 33% in NTG and 37% in HTG (both P<0.001), and cholesteryl ester transfer activity fell 59% (P<0.001) in HTG only. Rosuvastatin thus lowers CETP mass regardless of triglyceride phenotype but only suppresses CETP transfer activity in hypertriglyceridemic patients, alongside largely correcting their atherogenic lipoprotein abnormalities.
Original abstract
This randomised, double-blind, placebo-controlled crossover study evaluated the effects of rosuvastatin (40 mg/day for 8 weeks) on atherogenic apolipoprotein B-containing lipoprotein subfractions. Subjects, recruited based on raised plasma triglyceride (TG) or low-density lipoprotein cholesterol (LDL-C), were divided into normotriglyceridaemic (NTG, n = 13; TG < 2.0 mmol/l) and hypertriglyceridaemic (HTG, n = 16; TG > or = 2.0 mmol/l) groups. Similar reductions on rosuvastatin were observed for both groups in LDL-C (NTG -60%; HTG -56%), apoB (both -49%), intermediate-density lipoprotein (NTG -57%; HTG -54%) and LDL circulating mass (NTG -52%, HTG -58%) (all P < 0.001 versus placebo), i.e., these changes were phenotype independent. Phenotype dependency in response was observed in HTG relative to NTG in concentration of small dense LDL (LDL-III) (NTG -44%, P = NS; HTG -69%, P < 0.001), very-low-density lipoprotein1 (NTG -18%, P = NS; HTG 46%, P < 0.01), and remnant-like particle cholesterol (NTG -31%, P = NS; HTG -48%, P < 0.05). Rosuvastatin reduced cholesteryl ester transfer protein (CETP) by 33% in NTG and 37% in HTG (both P < 0.001); a reduction in cholesteryl ester transfer activity (-59%, P < 0.001) was observed in HTG only. Rosuvastatin therefore, in addition to lowering LDL and apoB-concentrations, largely corrected the TG and LDL abnormalities in subjects who had the propensity to develop the atherogenic lipoprotein phenotype.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.