Abstract
BackgroundLipoprotein-associated phospholipase A2 (Lp-PLA2) also known as serum platelet activating factor acetylhydrolase (PAF-AH) activity constitutes a novel risk marker for cardiovascular disease. Leukocytes constitute one main cellular source of circulating Lp-PLA2. The aim of the present study was to evaluate the association of both serum and leukocyte PAF-AH activities with fat distribution and lean tissue. One hundred healthy volunteers without cardiovascular disease history participated in this study (n = 52 men, 44 ± 13 years and n = 48 women, 43 ± 13 years). Body composition was assessed with dual-energy X-ray absorptiometry, while anthropometrical indices were also measured. The activity of Lp-PLA2 and levels of lipid and glycemic parameters were determined in fasting samples.ResultsMean Lp-PLA2 activity was 24.8 ± 4.5 and 19.6 ± 5.0 nmol/min/mL in men and women, respectively (P < 0.001). Mean activity of PAF-AH in leukocyte homogenates was 386 ± 127 pmol/min/mg and 292 ± 92 pmol/min/mg in men and women, correspondingly (P < 0.001). In multiple regression models upper and total adiposity measures were positively associated with Lp-PLA2 activity in men after adjusting for LDL-cholesterol, age, smoking, hs-CRP and physical activity, whereas no associations were found with PAF-AH leukocyte homogenates activity. Hierarchical analysis revealed that the variables with the highest explanatory ability of Lp-PLA2 activity in men, were DXA deriving L1–L4 region of interest and arms fat (increase in R2 = 0.136, P = 0.005 and increase in R2 = 0.118, P = 0.009, respectively), followed by trunk fat and total fat. In women, no association of body composition variables with Lp-PLA2 nor PAF-AH leukocyte homogenates activity was found.ConclusionLp-PLA2 activity is differentiated across levels of adiposity and topology of adipose tissue, whereas no association was found regarding PAF-AH leukocyte homogenates activity. Our findings suggest that Lp-PLA2 may compensate for the adiposity-associated increases in inflammatory and oxidative burden, in men.
Highlights
Lipoprotein-associated phospholipase A2 (Lp-PLA2) known as serum platelet activating factor acetylhydrolase (PAF-AH) activity constitutes a novel risk marker for cardiovascular disease
There was no significant difference between men and women regarding age, body mass index (BMI) and smoking habits, whereas differences in certain biochemical parameters and body composition measurements, such as total body fat and central adiposity were observed
PAF-AH in leukocyte homogenates was associated with LDL-cholesterol and Lipoprotein associated phospholipase A2 (Lp-PLA2) in women (r = 0.338, p = 0.013 and r = 0.278, p = 0.049), whereas in men no association was found between PAF-AH in leukocyte homogenates with lipid parameters or Lp-PLA2 activity
Summary
Lipoprotein-associated phospholipase A2 (Lp-PLA2) known as serum platelet activating factor acetylhydrolase (PAF-AH) activity constitutes a novel risk marker for cardiovascular disease. Its accumulation at the upper body compartments results in the infiltration of macrophages [1] and the concomitant production of pro-inflammatory, pro-oxidant and prothrombotic factors, such as tumor-necrosis factor alpha (TNF-α), interleukin-6 (IL-6), platelet activating factor (PAF), PAF-like molecules and oxidized phospholipids [2,3,4]. This local inflammatory burst characterized with tissue remodelling, macrophage activation and enhanced chemoattraction of leukocytes together with the predominance of a systemic low grade inflammatory state turn the adipose tissue into a key player in atherosclerosis progress and inflammation [5]. Its action goes hand in hand with the production of inflammatory molecules, such as lysophosphatidylcholine and oxidized non esterified fatty acids [7], which are proatherogenic
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