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：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.
摘要:目的: 研究蜕皮甾酮对非酒精性脂肪性肝病大鼠模型肿瘤坏死因子α(TNFα)与核因子κB(NFκB)表达的影响，并探索其可能的作用机制。 方法 :健康成年SD大鼠36只,随机分为正常对照组12只与实验组24只;正常对照组喂以普通基础饲料,实验组应用高脂饲料喂养。实验12周末时将造模成功的实验组大鼠随机分为模型组与蜕皮甾酮治疗组2个亚组,每组12只;正常对照组喂以普通基础饲料至16周,模型组继续应用改良高脂饲料喂养至16周,蜕皮甾酮治疗组大鼠在高脂饮食同时加用蜕皮甾酮灌胃。实验16周末时处死3组所有大鼠;检测肝脏指数,血清与肝组织生化指标及肝组织病理改变;ELISA法检测肝脏TNFα水平;免疫组化检测各组大鼠肝组织中核因子κB蛋白表达情况。 结果 :蜕皮甾酮治疗组血清胆固醇(TC)、丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)明显低于模型组(212±058比263±024,Plt;005;5336±1848比8460±3627,P＜005;14020±3595比24359±3638,P＜001);蜕皮甾酮治疗组与模型组相比肝组织丙二醛(MDA)水平降低明显(18454±1645比23928±2376,P＜001),超氧化物歧化酶(SOD)活力增加显著(942±052比518±043,P＜001),肝脏指数显著降低(435±037比504±046,P＜001)，肝组织脂肪变性程度和炎症活动度明显减轻(546±037比630±049,P＜001)。蜕皮甾酮治疗组与模型组相比TNFα与核因子κB水平明显减轻(4304±748比6156±727,2465±539比4504±746,P值均＜001)。 结论 :蜕皮甾酮具有改善高脂饮食诱发的非酒精性脂肪性肝病大鼠肝脏酶学功能,通过增加肝组织SOD的含量和减少MDA的含量来减轻肝组织氧化应激水平,减轻肝组织TNFα和核因子κB来减轻肝脏炎症,发挥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.
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 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.
ObjectiveTo investigate the value of proton magnetic resonance spectroscopy (1H-MRS), gradient dual-echo, and triple-echo sequences in the quantitative evaluation of treatment effect of fatty liver at 3.0T MR.MethodsThirty patients with fatty liver diagnosed by CT or ultrasound who admitted in Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital between August 2017 and May 2018, were enrolled and undergone gradient dual-echo, triple-echo, and 1H-MRS examination before and 3 months after treatment. The fat index (FI) and relative lipid content (RLC) were measured. Fatty liver index (FLI) was calculated from blood biochemical indicators, waist circumference, and BMI at the same time. With the reference standard of FLI, the results before and after treatment measured from MRI were analyzed.ResultsThere were significantly differences of FLI, FIdual, FItriple, and RLC before and after treatment (t=5.281, P<0.001; Z=–3.651, P<0.001; Z=–3.630, P<0.001; Z=–4.762, P<0.001), all indexes decreased after treatment. FIdual and FItriple were positively correlated with FLI before (rs=0.413, P=0.023; rs=0.396, P=0.030) and after treatment (rs=0.395, P=0.031; rs=0.519, P=0.003), the highest correlation factor was FItriple to FLI after treatment. There were no significant correlation between RLC and FLI before and after treatment (P>0.05).ConclusionsIt is feasible to quantitatively evaluate the treatment effect of fatty liver by using 1H-MRS, gradient dual-echo, and triple-echo sequences. Gradient triple-echo sequences has better accuracy, which is technically easy to implement and more suitable for clinical development.
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.
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.
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.