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.
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.
Non-alcoholic fatty liver disease (NAFLD) is one of the major chronic liver diseases that endanger human health. It is characterized by hepatic steatosis and absence of other causes of hepatic fat accumulation, such as alcohol abuse. The incidence of NAFLD is increasing year by year. However, the pathogenesis is still undefined. Porphyromonas gingivalis is a major periodontal pathogen of various periodontal disease. Apart from affecting periodontal health, Porphyromonas gingivalis is also related to the incidence of many systemic diseases. In recent years, Porphyromonas gingivalis is considered to be a risk factor of NAFLD. In this paper, the relationship between NAFLD and Porphyromonas gingivalis, as well as the possible pathogenesis are discussed.
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.
【摘要】 目的 研究2型糖尿病（type 2 diabetes mellitus，T2DM）合并非酒精性脂肪性肝病（non-alcoholic fatty liver disease， NAFLD）患者血漿脂肪細胞特異性脂肪酸結合蛋白（adipocyte-specific fatty acid-binding protein，A-FABP）的水平及其相關因素。 方法 2009年10月—2010年10月選取T2DM合并NAFLD組（A組）60例，未合并NAFLD組56例（B組）為研究對象。測定體質量指數（body mass index，BMI），檢測血脂、糖化血紅蛋白（hemoglobin A1c，HbA1c）等生化指標。放射免疫法測定空腹胰島素（fasting insulin，FINS），空腹C肽水平（fasting C-peptide，FCP），計算胰島素抵抗指數（homeostasis model of assessment-insulin resistance，HOMA-IR）、胰島素敏感指數（insulin sensitivity index，ISI），測定A-FABP、C反應蛋白（C-reaction protein，CRP）及腫瘤壞死因子-α（tumor necrosis factor-α，TNF-α）。 結果 與B組患者相比，A組患者其血漿A-FABP水平、BMI、腰圍、腰臀比、丙氨酸氨基轉移酶、門冬氨酸氨基轉移酶、CRP、TNF-α、FCP、FINS、總膽固醇、甘油三酯、Ln（HOMA-IR）升高，Ln（ISI）降低，差異有統計學意義（Plt;0.05）；兩組HbA1c差異無統計學意義（Pgt;0.05）。A-FABP水平變化與TNF-α、HOMA-IR、CRP呈正相關，與ISI呈負相關。 結論 T2DM伴NAFLD中，A-FABP升高與胰島素抵抗是并存的，且存在明顯相關關系，二者在疾病的發生發展中均可能具有重要的作用。【Abstract】 Objective To analyze the serum level of adipocyte-specific fatty acid-binding protein (A-FABP) in patients with type 2 diabetes mellitus (T2DM) complicated with non-alcoholic fatty liver disease (NAFLD), and its related factors. Methods From October 2009 to October 2010, 112 patients with T2DM were categorized into two groups: the group with NAFLD (group A) with 60 patients, and the group without NAFLD (group B) with 56 patients. Body mass index (BMI), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and hemoglobin A1c (HbA1c) were detected. Radioimmunoassay was carried out to measure fasting insulin (FINS) and fasting C-peptide (FCP), and homeostasis model of assessment-insulin resistance (HOMA-IR) and insulin sensitivity index (ISI) were calculated. At the same time, A-FABP, C-reaction protein (CRP) and tumor necrosis factor-α (TNF-α) were also detected. Results Compared with patients in group B, plasma levels of A-FABP, BMI, waistline, waist to hip ratio, ALT, AST, TG, TC, HDL-C, LDL-C, CRP, FCP, FINS, and HOMA-IR for patients in group A were all higher, while ISI was lower; and the differences in the above-mentioned parameters were statistically significant (Plt;0.05). The levels of HbA1c in the two groups were not significantly different (Pgt;0.05). The change of A-FABP level was positively correlated with TNF-α, HOMA-IR and CRP, while it wasnegatively correlated with ISI. Conclusions In patients with T2DM with NAFLD, there is an obvious correlation between the coexisting A-FABP rise and insulin resistance. Both of them played critical roles in the onset and developing of the disease.
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.
摘要:目的: 研究蛻皮甾酮對非酒精性脂肪性肝病大鼠模型腫瘤壞死因子α(TNFα)與核因子κB(NFκB)表達的影響，并探索其可能的作用機制。 方法 :健康成年SD大鼠36只,隨機分為正常對照組12只與實驗組24只;正常對照組喂以普通基礎飼料,實驗組應用高脂飼料喂養。實驗12周末時將造模成功的實驗組大鼠隨機分為模型組與蛻皮甾酮治療組2個亞組,每組12只;正常對照組喂以普通基礎飼料至16周,模型組繼續應用改良高脂飼料喂養至16周,蛻皮甾酮治療組大鼠在高脂飲食同時加用蛻皮甾酮灌胃。實驗16周末時處死3組所有大鼠;檢測肝臟指數,血清與肝組織生化指標及肝組織病理改變;ELISA法檢測肝臟TNFα水平;免疫組化檢測各組大鼠肝組織中核因子κB蛋白表達情況。 結果 :蛻皮甾酮治療組血清膽固醇(TC)、丙氨酸氨基轉移酶(ALT)和天門冬氨酸氨基轉移酶(AST)明顯低于模型組(212±058比263±024,Plt;005;5336±1848比8460±3627,P＜005;14020±3595比24359±3638,P＜001);蛻皮甾酮治療組與模型組相比肝組織丙二醛(MDA)水平降低明顯(18454±1645比23928±2376,P＜001),超氧化物歧化酶(SOD)活力增加顯著(942±052比518±043,P＜001),肝臟指數顯著降低(435±037比504±046,P＜001)，肝組織脂肪變性程度和炎癥活動度明顯減輕(546±037比630±049,P＜001)。蛻皮甾酮治療組與模型組相比TNFα與核因子κB水平明顯減輕(4304±748比6156±727,2465±539比4504±746,P值均＜001)。 結論 :蛻皮甾酮具有改善高脂飲食誘發的非酒精性脂肪性肝病大鼠肝臟酶學功能,通過增加肝組織SOD的含量和減少MDA的含量來減輕肝組織氧化應激水平,減輕肝組織TNFα和核因子κB來減輕肝臟炎癥,發揮防治非酒精性脂肪性肝病的作用。Abstract: Objective: To investigate the effect and possible mechanism of ecdysterone on the expression of tumor necrosis factoralpha (TNFα) and nuclear factor κ B (NFκB) in rats with nonalcoholic fatty liver disease of rats. Methods : A total of 36 male Sprague Dawley rats were randomly divided into two groups, who were fed with highfat diet (experimental group, n=24) and normal basic food (normal control, n=12) respectively. At the end of the 12th week, the experimental group was randomly divided into two subgroups: model group and ecdysterone group, each group contained 12 rats. From the 13th week, the rats in the normal control group and model group were lavaged with normal sodium, and the rats in the ecdysterone group were lavaged with ecdysterone at 10 mg·kg-1·d-1. At the end of the 16th week, all rats were weighed, narcotized, sacrificed, and the liver index, biochemical indicators in serum and liver tissues and the hepatic pathological changes were observed. The expression of TNFα was detected by ELISA and the expression of NFκB was measured by immunohistochemical staining. Results : At the end 16th week in ecdysterone group, the serum levels of cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were reduced markedly (212±058 vs 263±024 and 5336±1848 vs 8460±3627, both P＜005; 14020±3595 vs 24359±3638, P＜001); the tissue content of malondialdehyde (MDA) was decreased evidently (18454±1645 vs 23928±2376, P＜001), while the activity of superoxide dismutase (SOD) was enhanced notably (942±052 vs 518±043, P＜001); the liver index was decreased significantly in comparison with that inmodel group (435±037 vs 504±046, P＜001); the degree of fatty degeneration and inflammation were relieved dramatically (546±037 vs 630±049, P＜001). The expression of TNFα and the levels of NFκB were significantly lower (4304±748 vs 6156±727 and 2465±539 vs 4504±746, both P＜001) in ecdysterone group compared with model group. Conclusion : The effects of ecdysterone in preventing NAFLD in rats could be related to the increase of SOD content in hepatic tissue and the decrease of MDA content, tumor necrosis factorα and NFκB.
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.
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.
