HDL biology
Rosuvastatin lowered CETP activity and mass while raising HDL-C in metabolic syndrome patients (Atherosclerosis 2008)
Original title: Indices of reverse cholesterol transport in subjects with metabolic syndrome after treatment with rosuvastatin
In a randomized, placebo-controlled, crossover trial, 25 overweight subjects with metabolic syndrome received rosuvastatin 40 mg/day for 4 weeks to examine effects on reverse cholesterol transport. Rosuvastatin lowered plasma cholesterol by 44%, LDL cholesterol by 60%, and triglycerides by 38%, while HDL cholesterol rose from 0.97 to 1.05 mmol/L and the LpA-I HDL component rose from 39 to 45 mg/dL (both P<0.05). LCAT activity fell (0.55 to 0.35 nmol/mL/h), and CETP activity and mass both fell (89 to 80 nmol/L/h and 1.66 to 1.28 ug/mL, respectively, P<0.05). In vitro cholesterol efflux to activated-macrophage plasma fell from 7.1% to 6.2% (P<0.05), a difference that lost significance once apoB lipoproteins were removed, and efflux was paradoxically inversely correlated with HDL-C and LpA-I during placebo but not after rosuvastatin. The authors suggest these findings point to HDL dysfunction in metabolic syndrome, with statin treatment reducing efflux capacity alongside reduced apoB lipoproteins and reduced CETP and LCAT activity despite higher HDL cholesterol.
Original abstract
Objective: The effects of the statin, rosuvastatin on indices of reverse cholesterol transport were studied in a randomized, placebo-controlled, cross-over trial in 25 overweight subjects with defined metabolic syndrome.
Result: Four weeks' treatment with 40 mg/day rosuvastatin significantly reduced levels of plasma cholesterol (44%), LDL cholesterol (60%) and triglyceride (38%). HDL cholesterol (mean [S.D.]) rose (0.97[0.17] to 1.05[0.17]mmol/L; P<0.05) and the LpA-I component of HDL from 39[7] to 45[9]mg/dL (P<0.05). LCAT activity fell (0.55[0.13] to 0.35[0.07]nmol/mL/h; P<0.05); CETP activity and mass fell from 89[13] to 80[11]nmol//L/h and from 1.66[0.57] to 1.28[0.41]mug/mL respectively, (P<0.05). Cholesterol efflux in vitro (to plasmas from THP-1 activated cells) fell from 7.1[1.8]% (placebo) to 6.2[1.7]% (rosuvastatin); P<0.05, but when plasmas depleted of apoB lipoproteins were studied, the difference in efflux was no longer statistically significant. During placebo efflux was paradoxically inversely correlated with HDL-C (P=0.016) and LpA-I (P=0.035) concentrations but these correlations were absent after rosuvastatin.
Conclusions: The data suggest possible HDL dysfunctionality in subjects with metabolic syndrome. The reduced capacity of plasmas following statin treatment to stimulate cholesterol efflux in vitro occurred in association with reduction in apoB lipoproteins and reduced activities of CETP and LCAT, and despite increased levels of HDL cholesterol.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.