Utility of traditional and non-traditional lipid indicators in the diagnosis of nonalcoholic fatty liver disease in a Japanese population.

BACKGROUND: Traditional and non-traditional (TNNT) lipid indicators are known to be closely related to nonalcoholic fatty liver disease (NAFLD). This study's objective was to compare the degree of associations and diagnostic values of TNNT lipid indicators with NAFLD. METHODS: Participants were 14,251 Japanese adults who undergoing health checkups, and we measured and calculated 11 lipid indicators, including traditional lipid indicators such as high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG), as well as non-traditional lipid indicators such as TC/HDL-C ratio, LDL-C/HDL-C ratio, TG/HDL-C ratio, non-HDL-C, remnant cholesterol (RC), RC/HDL-C ratio and non-HDL-C/HDL-C ratio. The associations between these lipid indicators and NAFLD were assessed using multivariate logistic regression, and the performance of these lipid indicators in identifying NAFLD was analyzed by receiver operating characteristic (ROC) curves. RESULTS: After rigorous adjustment for potential confounders, multivariate logistic regression showed that all TNNT lipid indicators were independently associated with NAFLD, among which the RC/HDL-C ratio and RC had the strongest association with NAFLD. ROC analysis showed that non-traditional lipid indicators were superior to traditional lipid indicators in identifying NAFLD, especially in young adults and females. It is worth mentioning that the RC/HDL-C ratio was the best lipid indicator for identifying NAFLD with an area under the curve (AUC) of 0.82 and an optimal cut-off value of 0.43; in addition, TG/HDL-C ratio also had a high recognition performance for NAFLD. CONCLUSION: Overall, in the Japanese population, non-traditional lipid indicators had a higher diagnostic value for NAFLD compared to traditional lipid indicators, and lipid indicators alone had a lower diagnostic value for NAFLD than the ratio of two lipid indicators, with RC/HDL-C and TG/HDL-C being the best lipid indicators for identifying NAFLD.

Methylation Mediated Silencing of miR-155 Suppresses the Development of Preeclampsia In Vitro and In Vivo by Targeting FOXO3.

Preeclampsia (PE) is a common pregnancy-related syndrome characterized by chronic immune activation. This study is aimed at exploring the role of miR-155 in the inflammatory pathogenesis of PE. Placental tissues and peripheral blood were collected from all subjects. BSP detection analysis was performed to evaluate miR-155 methylation levels. ELISA was performed to measure the levels of inflammatory cytokines and MMP2 in serum samples and cellular supernatants. HTR-8/SVneo and JEG-3 cells were transfected with miR-155 mimic and the inhibitor to establish the overexpressed miR-155 and silenced miR-155 cell models, respectively. Treatment with 5-Aza was performed to alter the DNA methylation level of miR-155. The PE rat model was established after subcutaneous injection of NG-nitro-L-arginine methyl ester. The CCK-8 assay, TUNEL staining, and Transwell assay were performed. Reverse transcription-quantitative PCR, Western blot analysis, and immunohistochemical assay were used to analyze related gene expression levels. The luciferase reporter assay was used to investigate the direct interaction between FOXO3 and miR-155. Results showed that miR-155 was remarkably upregulated and inversely correlated with the promoter methylation level in the placental tissue from PE patients. The in vitro experiments indicated that miR-155 decreased viability, migration, and invasion, but increased apoptosis in trophoblast cells. FOXO3 was confirmed as the target of miR-155. Transfection of the miR-155 inhibitor suppressed inflammation and oxidative stress, but elevated proliferation, migration, and invasion of trophoblast cells, which were abolished by 5-Aza treatment or cotransfection with si-FOXO3. In summary, our data suggested that methylation-mediated silencing of miR-155 can inhibit the apoptosis, inflammation, and oxidative stress of trophoblast cells by upregulating FOXO3.