The class
Serum cholesterol efflux capacity is preserved or enhanced in genetically CETP-deficient patients (Clin Chim Acta 2008)
Original title: Cholesterol efflux from J774 macrophages and Fu5AH hepatoma cells to serum is preserved in CETP-deficient patients
Comparing genetically CETP-deficient subjects (two homozygous, one compound heterozygous, five heterozygous) with ten normolipidemic controls, researchers measured serum cholesterol acceptor capacity using two cell systems representing SR-BI-mediated and ABCA1-mediated efflux pathways. In homozygous CETP-null subjects, whole serum and HDL fraction 2 acceptor capacity toward Fu5AH hepatoma cells were 38% and 116% higher, respectively, than controls, indicating enhanced SR-BI-dependent efflux. Acceptor capacity toward ABCA1-upregulated J774 macrophages was similar between groups, showing that ABCA1-mediated efflux remains fully preserved despite complete or partial CETP deficiency, evidence against the concern that CETP inhibition might impair a key antiatherogenic HDL function.
Original abstract
Background: The role of CETP in the development of atherosclerosis is debatable, and few data exist regarding the total impact of CETP inhibition on cholesterol efflux.
Methods: Acceptor capacities of whole serum and HDL subfractions separated by HPLC were compared using 2 different cell systems. Subjects with CETP deficiency (2 homozygous, 1 compound heterozygous, and 5 heterozygous) were analyzed along with 10 normolipidemic controls. The fractional efflux from cholesterol-labeled Fu5AH hepatoma cells was determined to be SR-BI mediated. The efflux difference between control and liver X receptor (LXR) agonist-induced ABCA1-upregulated J774 macrophages was considered as a measure of ABCA1-mediated efflux.
Results: For the Fu5AH cell system, the total acceptor capacities of whole serum and HPLC-separated HDL fraction 2 obtained from the homozygous subjects were 38% and 116% higher than the corresponding values for the controls, respectively (p<0.05). For the J774 cell system, the total acceptor capacities of whole serum and HPLC-separated HDL fractions were similar among the CETP-deficient subjects and controls.
Conclusions: Serum from homozygous subjects with CETP-null defects exhibited enhanced acceptor capacity via an SR-BI dependent pathway, which is regulated by the middle HPLC-separated HDL fraction. Further, the cholesterol acceptor capacity of serum obtained from patients having complete and partial CETP deficiency was preserved via an ABCA1-dependent pathway.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.