Background: Platelet-activating-factor (PAF) is a lipid inflammatory mediator implicated
in liver disease. Its main biosynthetic enzymes are cytidine diphosphate (CDP)-choline:
1-alkyl-2-acetyl-sn-glycerol-cholinephosphotransferase (PAF-CPT) and acetyl-coenzyme A:
lyso-PAF-acetyltransferases (Lyso-PAF-AT). At the same time, PAF acetylhydrolase (PAF-AH)
and lipoprotein-associated phospholipase A2 (Lp-PLA2) degrade PAF.
Objective: To explore the relation of PAF metabolism with liver diseases and non-alcoholic fatty
liver disease, as reflected by the fatty liver index (FLI).
Methods: In 106 healthy volunteers, PAF concentration, the activity of its metabolic enzymes and
gamma-glutamyl transferase (GGT) were measured in whole blood, leukocytes and serum, respectively
and the FLI was calculated. Partial correlations and linear regression models were used.
Results: In males, serum GGT activity was positively correlated with abdominal fat (as assessed
by analysis of a manually defined region of interest in dual-energy X-ray absorptiometry), triacylglycerols,
bound-PAF and Lp-PLA2, while the FLI was positively correlated with Lp-PLA2 activity.
In females, serum GGT activity was negatively associated with high-density lipoprotein cholesterol
(HDL-C) (age adjusted correlations, all p<0.05). Lp-PLA2 was a significant determinant of serum
GGT activity in males after controlling for age, low- density lipoprotein cholesterol (LDL-C) and
abdominal fat. The addition of bound-PAF in the model significantly increased the explained
variance of serum GGT activity (total variance explanation 30%).
Conclusion: Bound-PAF and Lp-PLA2 activity predicted serum GGT activity while Lp-PLA2 was
also related to FLI. Our findings shed light on the metabolic pathways linking Lp-PLA2 to other
atherosclerosis and/or oxidative markers, such as HDL-C, LDL-C, GGT and FLI and underline the
important role of PAF.