Plasma cholesteryl ester transfer, but not cholesterol esterification, is related to lipoprotein-associated phospholipase A2: Possible contribution to an atherogenic lipoprotein profile

Context: Plasma lipoprotein-associated phospholipase A2(Lp-PLA2) 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 highdensity 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-PLA2in subjects with and without metabolicsyndrome (MetS). Design and Setting: In 68 subjects with MetS and 74 subjects without MetS, plasma Lp-PLA2mass, 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-PLA2was decreased (P<0.043) in MetS. CET was correlated positively with Lp-PLA2in subjects with and without MetS (P = 0.05 for both). EST and LCAT activity were unrelated to Lp-PLA2, despite a positive correlation between EST and CET (P = 0.001). After controlling for age, sex, and diabetes status, CET was determined by Lp-PLA2in the whole group (β = 0.245; P = 0.001), and in subjects with (β = 0.304; P = 0.001) and without MetS (β = 0.244; P = 0.006) separately, independently of triglycerides and CETP. Conclusions: PlasmaCETis related to Lp-PLA2in subjects withandwithout MetS.Theprocess of CET, but not EST, may be influenced by Lp-PLA2. These findings provide a rationale to evaluate whether maneuvers that inhibit Lp-PLA2will reduce CET, and vice versa to document effects of CETP inhibition on Lp-PLA2. Copyright

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