ObjectiveTo investigate the relationship between nonalcoholic fatty liver disease (NAFLD) and Helicobacter pylori (HP) infection. MethodsMedical examination data of healthy physical examination participates who underwent carbon 14 urea breath test for detection of HP and abdominal ultrasound examination between March and June 2015 were analyzed. Cross sectional analysis was carried out. Based on the diagnostic criteria of NAFLD, the subjects were divided into two groups: NAFLD group and normal control group. HP infection was compared between the two groups. Logistics regression analysis was performed to analyze the relationship between HP infection and NAFLD. ResultsThe proportion of men, age, weight, body mass index (BMI), waistline, alanine aminotransferase (ALT), aspartate aminotransferase, glutamyl transferase, albumin, fasting blood-glucose (GLU), total cholesterol triacylglycerol (TG), low density lipoprotein-cholesterol, and blood pressure were all significantly higher in the NAFLD group than the control group (P < 0.05), while height and high density lipoprotein-cholesterol were significantly lower in the NAFLD group (P < 0.05). The detection rate of NAFLD in males was higher than that in females. The detection rates of NAFLD in different age groups were significantly different, and the highest detection rate of NAFLD was in the age group of 50-59 years old (P < 0.05). The rate of HP infection was not significantly different in subjects of different ages and genders (P > 0.05). The rate of HP infection in the NAFLD group was significantly higher than those of the control group in age groups of 18-29, 30-39, 40-49, 50-59, and 70-79 years old (P < 0.05). The logistic regression analysis revealed that age, HP infection, TG, ALT, BMI, GLU, and diastolic pressure were correlated with NAFLD (P < 0.05). ConclusionHP infection may be a risk factor in the development of NAFLD.
ObjectivesTo systematically review the association between serum high sensitivity C-reactive protein (HS-CRP) and nonalcoholic fatty liver disease (NAFLD).MethodsPubMed, EMbase, The Cochrane Library, CNKI, SinoMed and WanFang Data databases were electronically searched to collect case-control studies on the association between HS-CRP and NAFLD from inception to October, 2019. Two reviewers independently screened literature, extracted data and assessed risk of bias of included studies. Meta-analysis was then performed using RevMan 5.3 software.ResultsA total of 22 case-control studies involving 5 825 subjects were included. The results of meta-analysis showed that HS-CRP levels in NAFLD group were higher than non-NAFLD group (SMD=1.25, 95%CI 0.81 to 1.68, P<0.000 01). The results of subgroup analysis showed that, HS-CRP levels in NAFLD group were higher in Asian region (SMD=1.32, 95%CI 0.82 to 1.83, P<0.000 01), however not in American region (SMD=0.48, 95%CI −0.02 to 0.98, P=0.06). HS-CRP levels in NAFLD group were higher in BMI≥30 kg/m2 group (SMD=0.37, 95%CI 0.19 to 0.54, P<0.000 1), however not in BMI<30 kg/m2 group (SMD=1.19, 95%CI −0.28 to 2.66, P=0.11). Additionally, HS-CRP levels in NAFLD group were higher with or without diabetes (SMD=0.86, 95%CI 0.49 to 1.24, P<0.000 01; SMD=1.47, 95%CI 0.84 to 2.10, P<0.000 01).ConclusionsCurrent evidence shows that NAFLD patients have higher levels of HS-CRP than non-NAFLD patients, and are affected by high levels of BMI and geographical regions. Therefore, HS-CRP may play important roles in the non-invasive field of NAFLD detection. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusions.
Objective To systematically review the effect of intermittent fasting on non-alcoholic fatty liver disease (NAFLD). Methods The PubMed, EMbase, Web of Science, Cochrane Library, CNKI, WanFang Data and CBM databases were electronically searched to collect studies on the effect of intermittent fasting on NAFLD from inception to October 1, 2022. Two researchers independently screened the literature, extracted data and evaluated the risk of bias of the included studies. R software was then used for meta-analysis. Results A total of 7 studies were included. The results of meta-analysis showed that intermittent fasting could reduce liver fibrosis (MD=−0.93, 95%CI 1.67 to 0.19, P<0.05), the levels of glutamic oxaloacetic transaminase (MD=−8.96, 95%CI −11.83 to −6.10, P<0.05), glutamyl transpeptidase (MD=−7.86, 95%CI −12.00 to −3.73, P<0.05), and inflammatory molecules (MD=−2.03, 95%CI −3.69 to −0.36, P<0.05). In addition, it reduced dietary (total energy) intake (MD=−255.99, 95%CI −333.15 to −178.82, P<0.05), body weight (MD=−2.42, 95%CI −3.81 to −1.02, P<0.05), BMI (MD=−0.52, 95%CI −0.92 to −0.13, P<0.05) and fat mass (MD=−2.37, 95%CI −4.17 to −0.57, P<0.05). Conclusion Current research evidence shows that intermittent fasting can improve NAFLD and help patients lose weight. Due to the limited quantity and quality of the included studies, more high-quality studies are needed to verify the above conclusion.
ObjectiveTo investigate whether there is a causal relationship between the intake of milk or coffee and the risk of non-alcoholic fatty liver disease (NAFLD). MethodsUsing a two-sample Mendelian randomization approach, single nucleotide polymorphisms (SNPs) associated with milk or coffee intake were used as instrumental variables, and genome-wide association study data on NAFLD were used as the outcome event. Inverse-variance weighted (IVW) and MR-Egger methods were employed to investigate the causal effect of milk or coffee intake on the risk of NAFLD. ResultsBoth analyses indicated no causal association between milk or coffee intake and the risk of NAFLD (P>0.05). Sensitivity analysis indicated the robustness of the main findings, with no outliers, heterogeneity, horizontal pleiotropy, or significant influence of individual SNPs. ConclusionThis study does not support a causal relationship between the intake of milk or coffee and the risk of NAFLD.