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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 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-PLA2 in subjects with and without metabolic syndrome (MetS).    Design and Setting:  In 68 subjects with MetS and 74 subjects without MetS, plasma Lp-PLA2 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 &amp;lt; 0.001 for all), and CETP (P = 0.030) were increased, and Lp-PLA2 was decreased (P = 0.043) in MetS. CET was correlated positively with Lp-PLA2 in subjects with and without MetS (P &amp;lt; 0.05 for both). EST and LCAT activity were unrelated to Lp-PLA2, despite a positive correlation between EST and CET (P &amp;lt; 0.001). After controlling for age, sex, and diabetes status, CET was determined by Lp-PLA2 in the whole group (β = 0.245; P &amp;lt; 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:  Plasma CET is related to Lp-PLA2 in subjects with and without MetS. The process of CET, but not EST, may be influenced by Lp-PLA2. These findings provide a rationale to evaluate whether maneuvers that inhibit Lp-PLA2 will reduce CET, and vice versa to document effects of CETP inhibition on Lp-PLA2.

the journal of clinical endocrinology and metabolism/journal of clinical endocrinology and metabolism

Plasma Cholesteryl Ester Transfer, But Not Cholesterol Esterification, Is Related to Lipoprotein-Associated Phospholipase A2: Possible Contribution to an Atherogenic Lipoprotein Profile