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.
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.
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.
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.
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.