Plasma Cholesteryl Ester Transfer, But Not Cholesterol Esterification, Is Related to Lipoprotein-Associated Phospholipase A(2): Possible Contribution to an Atherogenic Lipoprotein Profile

Robin P. F. Dullaart*, Alexander Constantinides, Frank G. Perton, Jeroen J. J. van Leeuwen, Joost L. van Pelt, Rindert de Vries, Arie van Tol

*Bijbehorende auteur voor dit werk

OnderzoeksoutputAcademicpeer review

14 Citaten (Scopus)
150 Downloads (Pure)

Samenvatting

Context: Plasma lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) predicts incident cardiovascular disease and is associated preferentially with negatively charged apolipoprotein B-containing lipoproteins. The plasma cholesteryl ester transfer (CET) process, which contributes to low high-density lipoprotein cholesterol and small, dense low-density lipoproteins, is affected by the composition and concentration of apolipoprotein B-containing cholesteryl ester acceptor lipoproteins.

Objective: We tested relationships of CET with Lp-PLA(2) in subjects with and without metabolic syndrome (MetS).

Design and Setting: In 68 subjects with MetS and 74 subjects without MetS, plasma Lp-PLA(2) mass, cholesterol esterification (EST), lecithin: cholesterol acyltransferase (LCAT) activity level, CET, CET protein (CETP) mass, and lipoproteins were measured.

Results: EST, LCAT activity, CET (P <0.001 for all), and CETP (P = 0.030) were increased, and Lp-PLA(2) was decreased (P = 0.043) in MetS. CET was correlated positively with Lp-PLA(2) in subjects with and without MetS (P <0.05 for both). EST and LCAT activity were unrelated to Lp-PLA(2), despite a positive correlation between EST and CET (P <0.001). After controlling for age, sex, and diabetes status, CET was determined by Lp-PLA(2) in the whole group (beta = 0.245; P <0.001), and in subjects with (beta = 0.304; P = 0.001) and without MetS (beta = 0.244; P = 0.006) separately, independently of triglycerides and CETP.

Conclusions: Plasma CET is related to Lp-PLA(2) in subjects with and without MetS. The process of CET, but not EST, may be influenced by Lp-PLA(2). These findings provide a rationale to evaluate whether maneuvers that inhibit Lp-PLA(2) will reduce CET, and vice versa to document effects of CETP inhibition on Lp-PLA(2). (J Clin Endocrinol Metab 96: 1077-1084, 2011)

Originele taal-2English
Pagina's (van-tot)1077-1084
Aantal pagina's8
TijdschriftJournal of Clinical Endocrinology and Metabolism
Volume96
Nummer van het tijdschrift4
DOI's
StatusPublished - apr-2011

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