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Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined. mRNA and protein levels of FABP1 were measured by quantitative RT-PCR (qPCR) and Western blotting. HBx-mediated FABP1 regulation was evaluated by luciferase assay, coimmunoprecipitation, and chromatin immunoprecipitation. Hepatic lipid accumulation was measured by using Oil-Red-O staining and the triglyceride level. It was found that expression of FABP1 was increased in HBV-producing hepatoma cells, the sera of HBV-infected patients, and the sera and liver tissues of HBV-transgenic mice. IMPORTANCEAccumulating evidence from epidemiological and experimental studies has indicated that chronic HBV infection is associated with hepatic steatosis. However, the molecular mechanism underlying HBV-induced pathogenesis of hepatic steatosis still remains to be elucidated. In this study, we found that expression of liver fatty acid binding protein (FABP1) was dramatically increased in the sera of HBV-infected patients and in both sera and liver tissues of HBV-transgenic mice. Forced expression of HBx led to FABP1 upregulation, whereas knockdown of FABP1 remarkably diminished lipid accumulation in both in vitro and in vivo models. It is possible that HBx promotes hepatic lipid accumulation through upregulating FABP1 in the development of HBV-induced nonalcoholic fatty liver disease. Therefore, inhibition of FABP1 might have therapeutic value in steatosis-associated chronic HBV infection. H epatitis B virus (HBV) infection is a serious health problemworldwide, causing acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (1). Emerging evidence from epidemiological and experimental studies suggests that chronic HBV infection, as well as HCV infection, is associated with hepatic steatosis (2, 3). The frequency of hepatic steatosis in subjects with a chronic HBV infection ranges from 27 to 51% (4). Furthermore, HBV X protein (HBx) is known to cause hepatic lipid deposition by inhibiting the secretion of apolipoprotein B (5). A previous report showed that the increased HBx expression can cause lipid accumulation in hepatocytes, likely mediated by sterol regulatory element binding protein 1 and peroxisome proliferator-activated receptor ␥ (PPAR␥) (4). The molecular mechanism by which HBV induces the pathogenesis of hepatic steatosis remains elusive. Using fluorescent two-dimensional difference gel electrophoresis and matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis, we found that the protein level of liver fatty acid binding protein (L-FABP ...

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Combined Streptococcus and Prevotella abundance is regarded as an independent species prognostic biomarker in ESCC patients.

We investigated the possible association between genetic variants in the Patatin like phospholipase-3 (PNPLA3) gene and nonalcoholic fatty liver disease (NAFLD) in a Han Chinese population. We evaluated twelve tagging single-nucleotide polymorphisms (tSNPs) of the PNPLA3 gene in a frequency matched case–control study from Fuzhou city of China (553 cases, 553 controls). In the multivariate logistic regression analysis, the rs738409 GG or GC, and rs139051 TT genotypes were found to be associated with increased risk of NAFLD, and a significant trend of increased risk with increasing numbers of risk genotype was observed in the cumulative effect analysis of these single nucleotide polymorphisms. Furthermore, haplotype association analysis showed that, compared with the most common haplotype, the CAAGAATGCGTG and CGAAGGTGTCCG haplotypes conferred a statistically significant increased risk for NAFLD, while the CGGGAACCCGCG haplotype decreased the risk of NAFLD. Moreover, rs738409 C>G appeared to have a multiplicative joint effect with tea drinking (P<0.005) and an additive joint effect with obesity (Interaction contrast ratio (ICR) = 2.31, 95% CI: 0.7–8.86), hypertriglyceridemia (ICR = 3.07, 95% CI: 0.98–5.09) or hypertension (ICR = 1.74, 95% CI: 0.52–3.12). Our data suggests that PNPLA3 genetic polymorphisms might influence the susceptibility to NAFLD development independently or jointly in Han Chinese.

Background: Non-alcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disease nowadays. Changes in diet and lifestyle have led to a dramatic increase in the prevalence of NAFLD around the world. This meta-analysis is to investigate the efficacy of physical activity intervention on liver-specific endpoints in the population with NAFLD, including hepatic enzyme, serum lipid, glucose metabolism and intra-hepatic lipid. Methods: PubMed and China National Knowledge Infrastructure (CNKI) databases were searched for randomized clinical trials of physical activity intervention on NAFLD patients through April 20th, 2019. Effect sizes were reported as standardized mean difference (SMD) and 95% confidence intervals (CI). Quality of included studies was assessed according to the Cochrane risk of bias tool. Meta-analyses were conducted using random-effect or fixed-effect models depending on the significance of heterogeneity. Subgroup analyses according to types and duration of physical activity were conducted to investigate clinical variability. Results: Nine studies with a cumulative total of 951 participants met selection criteria. Physical activity was found associated with small reductions in hepatic enzyme parameters: ALT (SMD-0.17, 95% CI:-0.30 to − 0.05), AST (SMD-0.25, 95% CI: − 0.38, − 0.13) and GGT (SMD-0.22, 95% CI: − 0.36, − 0.08). Significant small improvements were also found in serum lipid parameters including TC (SMD = − 0.22, 95% CI: − 0.34, − 0.09), TG (SMD = − 0.18, 95% CI: − 0.31 to − 0.06) and LDL-C (SMD = − 0.26, 95% CI: − 0.39 to − 0.13). Significant improvement was also found in intrahepatic lipid content (SMD = − 0.21, 95% CI: − 0.36 to − 0.06) There was no difference between physical intervention group and control group in HDL and three glucose metabolism parameters. Subgroup analysis suggested both aerobic exercise alone and resistance exercise alone can improve most liver function and longer period of exercise generally had better improvement effect.

ObjectivesNut consumption has been associated with a lower risk of type 2 diabetes, metabolic syndrome and insulin resistance. However, its effect on the risk of non-alcoholic fatty liver disease (NAFLD) is unknown. Therefore, we investigated the relationship between nut consumption and NAFLD risk.Setting and participantsWe conducted a retrospective case-control study including 534 patients diagnosed with NAFLD and 534 controls matched by sex and age (±5 years) from the Affiliated Nanping First Hospital of Fujian Medical University in China.Main outcome measuresInformation on dietary intake was collected using a semiquantitative food frequency questionnaire and nut consumption was calculated. Nut consumption was categorised using quartiles based on the distribution of daily nut intake of the controls. Binary logistic regression models were used to estimate ORs and the 95% CIs for the association between nut consumption and NAFLD risk.ResultsAfter adjusting for potential confounding variables, nut consumption was not associated with NAFLD risk in the overall sample. When the fully adjusted model was stratified by sex, a significant inverse association was found between high nut consumption and NAFLD only among the men in the highest quartile (OR=0.43; 95% CI 0.26 to 0.71;Ptrend =0.01). The inverse association of nut consumption with NAFLD risk in men remained significant after controlling for other known or suspected risk factors for NAFLD.ConclusionsDiets with a higher intake of nuts may be associated with a decreased risk of NAFLD, particularly in men.

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