Association of Lipoprotein-Associated Phospholipase A2 with the Prevalence of Nonalcoholic Fatty Liver Disease: A Result from the APAC Study

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a worldwide chronic liver disease. Few studies have investigated the association between NAFLD and Lipoprotein-associated phospholipase A2 (Lp-PLA2), a unique enzyme correlated with oxidative stress. The aim of this study was to assess the relationship between Lp-PLA2 and NAFLD in a Chinese community-based cohort. A total of 1587 adults aged ≥40 years were enrolled in the current study. Participants underwent a standardized evaluation. The serum Lp-PLA2 concentration was measured by ELISA and NAFLD was diagnosed by ultrasonography. Multivariable logistic regression was used to assess the association between Lp-PLA2 and NAFLD. Increased Lp-PLA2 levels were significantly associated with decreased NAFLD prevalence after adjusting for other potential confounders. The adjusted ORs of NAFLD in Q2, Q3 and Q4 compared with Q1 were 0.88 (0.64–1.21), 0.71 (0.51–0.98) and 0.67 (0.48–0.95), respectively (P < 0.05). Furthermore, the adjusted ORs of moderate and heavy NAFLD in Q2, Q3 and Q4 compared to Q1 were 0.64 (0.41–1.01), 0.48 (0.29–0.80) and 0.47 (0.28–0.79), respectively (P < 0.01). In conclusions, increased Lp-PLA2 levels were independently associated with decreased NAFLD prevalence.

Energy Intake and Plasma Adiponectin as Potential Determinants of Lipoprotein‐Associated Phospholipase A2 Activity: A Cross‐Sectional Study

“…However, Lp-PLA 2 activity was negatively associated with cardiometabolic risk factors that have not been previously studied, in particular, with markers of liver function, SGOT, and SGPT. The negative associations of Lp-PLA 2 activity with SGOT and SGPT may be supported by two studies (de Oliveira et al, 2015;Liu et al, 2018); in a recently published community-based study, increased Lp-PLA 2 levels were associated with decreased alanine aminotransferase levels and a decreased NAFLD prevalence (Liu et al, 2018); results from an animal study suggested that circulating PAF -the primary substrate of Lp-PLA 2 -modulates hepatic inflammation and fat accumulation and may protect against liver dysfunction and dyslipidemia (de Oliveira et al, 2015).…”

Association between Helicobacter pylori infection and non-alcoholic fatty liver disease in North Chinese: a cross-sectional study

“…All of the examiners were blind to the health status and laboratory test results of the participants. NAFLD was diagnosed on the basis of characteristic sonographic features, including hepatorenal echo contrast, liver parenchymal brightness, deep beam attenuation, and vessel blurring 28 .…”

Lipidomics in non-alcoholic fatty liver disease

“…As concerns the LPC levels in plasma, an impairment either on LCAT activity or PLA2 activity, as well as an increased turnover of LPC to PC or lysophosphatidic acid and sphingosine-1-phosphate are probable causes of diminished LPC levels in plasma. In fact, lipoprotein associated phospholipase A2 levels were found to be decreased in patients with NAFLD, whereas LCAT activity was higher in subjects with NAFLD, as inferred from a Fatty Liver Index > 60[ 49 , 50 ]. Moreover, a study in mice reported lower levels of palmitoyl-, stearoyl-, and oleoyl-LPCs in NASH compared to animals with NAFL, suggesting that the activity of lyso-PC acyltransferase, that catalyzes the recycle of LPCs to PC, is elevated in NASH[ 51 ].…”