4.7 Article

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

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JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
卷 96, 期 4, 页码 1077-1084

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ENDOCRINE SOC
DOI: 10.1210/jc.2010-2139

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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)

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