摘要:目的：探讨成都地区体检人群中丙氨酸氨基转移酶（ALT）升高率与其升高的相关因素,为正确分析引起ALT升高的原因提供相关依据。方法:以参与体检的8734名体检人群为研究对象,收集身高、体重、血压、丙氨酸氨基转移酶、空腹血糖、高密度脂蛋白、低密度脂蛋白、总胆固醇、甘油三酯、血清HBsAg、脂肪肝及胆石症等相关资料进行分析。结果:在全部体检人群中,ALT升高率为1011%,男性ALT升高率为13.70%,女性ALT升高率为6.30%,男性明显高于女性（Plt;0001）；ALT升高组的年龄均数小于ALT正常组（Plt;0001）；在ALT升高的受检者中,脂肪肝、高脂血症、肥胖、糖尿病、胆囊结石、饮酒及乙肝等患病率均高于ALT正常组受检者（Plt;005）。结论:脂肪肝、糖脂代谢紊乱及乙肝是体检人员ALT升高的主要原因；男性和低龄也是体检者ALT升高的危险因素。Abstract: Objective: To investigate the prevalence and relative factors of elevated serum alanine aminotransferase(ALT) levels and providescientific bases for its causes analysis in physical examination people in Chengdu. Methods: Subjects who received medical examination in physical examination center of west China hospital were screened in this study. The information of height, body weight, blood pressure, serum ALT, fasting plasma glucose, highdensity lipoprotein cholesterol, lowdensity lipoprotein cholesterol, total cholesterol, triglyceride, hepatitis B surface antigen (HBsAg) statue, fatty liver and cholelithiasis were collected and analyzed. 〖WT5”HZ〗Results:〖WT5”BZ〗 A total of 8734 cases were included in this study. The total prevalence of elevated ALT was observed in 1011%, including 137% in man and 63% in woman, and this difference between man and woman was statistic significant (P＜0001). The mean age of ALT elevated group was obvious lower than that of normal ALT group (P＜0001). Interesting, the occurrence rates of fatty liver, hyperlipidemia, obesity, diabetes,gallstones, drinking and positive hepatitis B surface antigen in ALT elevated group were all significant higher than that in normal ALT group (P＜005). Conclusion: Fatty liver, glyeolipid metabolism disorder, and hepatitis B were main reasons of elevated ALT. Male and young cases were both high risk of elevated ALT in this study.
ObjectiveTo summarize the changes of gut microbiota after cholecystectomy, the mechanisms of changes, and the relation with colorectal cancer, nonalcoholic fatty liver disease and post-cholecystectomy syndrome after cholecystectomy, in order to provide new ideas for the perioperative management of patients undergoing cholecystectomy. MethodThe studies related to gut microbiota after cholecystectomy at home and abroad were searched and analyzed for review. ResultsThe cholecystectomy disrupted the liver–bile acid–gut flora axis of the patients, and the composition and diversity of the gut microbiota of the patients were altered, and the alteration might lead to the occurrence of colorectal cancer, nonalcoholic fatty liver disease, and post-cholecystectomy syndrome, but the exact mechanism remained unclear. ConclusionsThe balance of intestinal microecology is disrupted after cholecystectomy, and the relation between cholecystectomy and gut microbiota may provide new ideas for the perioperative management of cholecystectomy patients and the prevention and treatment of diseases or symptoms after cholecystectomy, but the effect of cholecystectomy on gut microbiota and the relation with diseases or symptoms still need to be further studied.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
ObjectiveTo expounded the relationship between phenylalanine, tyrosine and their metabolites and non-alcoholic fatty liver disease (NAFLD). MethodThe literatures related to NAFLD in recent years were reviewed and analyzed. ResultThe levels of phenylalanine, tyrosine and their metabolites had changed significantly in the occurrence and development of NAFLD, and could lead to the progress of NAFLD by affecting the related pathways of lipid metabolism. ConclusionPhenylalanine, tyrosine and their related metabolites are associated with NAFLD, but the specific pathogenesis is still unclear.
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 summarize the mechanism of endoplasmic reticulum stress (ERS) in liver diseases. MethodWe sorted out and summarized the studies related to ERS and liver diseases in recent years. ResultsEndoplasmic reticulum plays important roles in protein folding, calcium ion storage, and lipid synthesis in cells. ERS will be induced when the number of misfolded/unfolded proteins in the endoplasmic reticulum increases or the calcium ion homeostasis is unbalanced. The endoplasmic reticulum regulates the unfolded protein response through three transmembrane receptor proteins to initiate corresponding pathways for restoring endoplasmic reticulum homeostasis. Prolonged stress can lead to metabolic disorders. Mild ERS can promote the progression of hepatocellular carcinoma, and continuous ERS will induce cell apoptosis and play an anti-tumor effect; ERS can promote lipid accumulation in non-alcoholic fatty liver disease and aggravate the progression of the disease; in hepatic ischemia reperfusion injury, ERS activation will aggravate liver damage. Meanwhile, ERS activation plays an important pathogenic role in the pathogenesis of drug-induced liver injury. ConclusionERS plays a crucial regulatory role in the occurrence and development of liver-related diseases, providing a theoretical basis and new approach for targeted ERS therapy in liver diseases.
Objectives To systematically review the association between TM6SF2 (transmembrane six superfamily member 2- rs58592426) polymorphism and liver lesion and the severity of liver fibrosis. Methods We electronically searched databases including PubMed, CNKI, WanFang Data and CBM from inception to January 27, 2016, to collect cross-sectional studies about the association between the TM6SF2 polymorphism and the liver lesion and the severity of liver fibrosis. Two reviewers independently screened literature, extracted data and assessed the methodological quality included studies. Then, meta-analysis was performed using Stata 12.0 software. Results A total of 23 studies including 96 594 patients were included. The results of meta-analysis showed that: TM6SF2 polymorphism was associated with increased risk of the severity of liver fibrosis, the levels of TG, TC and LDL-C (all P values < 0.05). Carriers of the T allele showed lower levels of TG, TC, and LDL-C. Carriers of the T allele revealed higher levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) when compared with homozygous EE. Conclusion TM6SF2 polymorphism is associated with lipid traits in different population, the variants shows lower levels of lipid traits in blood serum and increases the risk of the severity of liver fibrosis and liver lesion.
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.
ObjectiveTo understand the current research progress on the role of hydrogen sulfide (H2S) in liver diseases. MethodThe relevant literature on the role of H2S in the liver diseases published in recent years was retrieved and reviewed. ResultsCurrent research focused primarily on exploring the mechanisms of H2S in various liver diseases. Studies had shown that H₂S played an important role in the occurrence and development of liver diseases through mechanisms such as antioxidative stress, anti-inflammatory effects, regulation of autophagy, endoplasmic reticulum stress, angiogenesis, and cell death. ConclusionsBy supplementing exogenous H2S, adjusting the gut microbiota, or inhibiting key enzymes involved in H₂S synthesis, the concentration of H2S in the body can be modulated, providing new strategies for treating liver diseases. However, the related mechanisms are still controversial. Future research should further investigate the specific role of H2S in different liver diseases and how to precisely control its level in the body to achieve targeted drug delivery.
Objective To investigate the incidence and risk factors of non-alcoholic fatty liver disease (NAFLD) in patients with myocardial infarction. Methods A total of 634 patients with myocardial infarction from Beijing Anzhen Hospital were asked to take liver and gallbladder ultrasonography during hospitalization, and then divided into the NAFLD and non-NAFLD groups. The incidence and risk factors of the two groups were then analyzed. Results The incidence of NAFLD was 52.2% (331/634). Both body mass index (BMI) and serum alanine aminotransferase of the NAFLD group were higher than those of non-NAFLD group, with significant difference (Plt;0.05). The incidence of NAFLD was positively increased following the severity of coronary diseases (χ2=7.275, P=0.03). The result of multivariable logistic regression analysis showed BMI, multi-vessel lesions of coronary disease, and left main coronary artery lesion were the independent risk factors of NAFLD. Conclusion The myocardial infarction patients who are particularly complicated by overweight, multi-vessel lesions and left main coronary artery lesion have a higher incidence of NAFLD.