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


METHODS
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 (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
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).
Department of Endocrinology, University of Groningen and University Medical Center Groningen, 9700 RB Groningen, The Netherlands. r.p.f.dullaart@int.umcg.nl
Robin P F
RP
Dullaart
Alexander
A
Constantinides
Frank G
FG
Perton
Jeroen J J
JJ
van Leeuwen
Joost L
JL
van Pelt
Rindert
R
de Vries
Arie
A
van Tol
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism / Q000502:physiology*; D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000378:metabolism*; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D053480:Cholesterol Ester Transfer Proteins / Q000378:metabolism*; D002788:Cholesterol Esters / Q000097:blood* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000378:metabolism; D004951:Esterification / Q000502:physiology; D005260:Female; D006801:Humans; D016014:Linear Models; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications / Q000378:metabolism; D055442:Metabolome / Q000502:physiology; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase