scholarly journals Serum microRNA-34a is potential biomarker for inflammation in nonalcoholic fatty liver disease

2017 ◽  
Vol 10 (2) ◽  
pp. 163-171 ◽  
Author(s):  
Puth Muangpaisarn ◽  
Kanisa Jampoka ◽  
Sunchai Payungporn ◽  
Naruemon Wisedopas ◽  
Chalermrat Bunchorntavakul ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Characteristic Curve ◽  
Control Group ◽  
Liver Inflammation ◽  
Apoptosis Pathway ◽  
Nonalcoholic Fatty Liver ◽  
Potential Biomarker

Abstract Background MicroRNA-34a (miR-34a) contributes to liver injury through an apoptosis pathway. Objective To determine the correlation between serum miR-34a and liver inflammation as assessed by nonalcoholic fatty liver disease (NAFLD) activity score (NAS). Method We included a cross-selectional study of 50 patients with NAFLD in this observational study and confirmed diagnosis by liver biopsy, with NAS grading. A control group comprised 23 healthy individuals without chronic liver disease. Serum miR-34a was assayed using a real-time quantitative PCR (Applied Biosystems). Result The mean age of NAFLD patients was 46.0 ± 13.7 years, and 52% were female. Metabolic syndrome was found in 76%. Liver histopathology showed that 54% of patients had NAS ≥4 and significant fibrosis (≥2) was found in 22%. Serum levels of miR-34a were significantly correlated with NAS (r = 0.39, P = 0.005), and the degree of steatosis (r = 0.28, P = 0.049), ballooning (r = 0.30, P = 0.034), and fibrosis (r = 0.39, P = 0.005). Serum miR-34a in patients with NAS ≥4 was significantly higher than in those with NAS <4 (P = 0.011) and controls (P < 0.001). There was no significant correlation between serum miR-34a and other variables. The area under receiver operating characteristic curve for serum miR-34a comparing patients with NAS ≥4 and with NAS <4 was 0.67 (95% CI 0.52, 0.82). Conclusion Serum level of miR-34a has a significant fair to good correlation with NAS and may serve as a biomarker of liver inflammation and fibrosis in patients with NAFLD.

scholarly journals GOUT AND NONALCOHOLIC FATTY LIVER DISEASE: EFFECT OF ENTEROSORPTION’S ADDITION TO COMMON TREATMENT

2020 ◽  
Vol 5 (2) ◽  
pp. 40-46
Author(s):  
U. O. Mudra
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Pathological Process ◽  
Control Group ◽  
Nonalcoholic Fatty Liver ◽  
Group 2 ◽  
Disease Effect ◽  
Basic Treatment

Background. Gout is still one of the major health problems despite significant advances in treatment in recent years. It has been proved that pathogenetic mechanisms of development and progression of gout are associated with nonalcoholic fatty liver disease. Complex pathogenic treatment of patients aimed at different parts of the pathological process has recently been supplemented with the enterosorbents. Objective. The aim of the research is to study the clinical features of gout with concomitant nonalcoholic fatty liver disease (NAFLD) and to evaluate the effect of carbon enterosorbent on its course. Methods. 123 patients were involved in the study. They were divided into 2 groups: group 1 included patients with gout without liver damage, and group 2 included patients with concomitant NAFLD. Each of these groups was divided into subgroups, in which the patients received carbon enterosorbent carboline plus basic treatment. The control group consisted of 30 healthy persons. Anamnesis, physical examination, uric acid (UA), C-reactive protein (CRP) content, erythrocyte sedimentation rate (ESR) in serum were determined. Gout activity was evaluated using the Gout Activity Score (GAS). Results. Basic treatment in combination with carbon enterosorbent contributed to faster cure of intoxication, pain and joint syndromes, as well as decrease of the inflammatory process activity. Conclusions. The course of gout in the patients with concomitant NAFLD is more severe. Adding of carbon granular enterosorbent carboline in the complex treatment of patients with gout with or without concomitant NAFLD in the exacerbation phase contributes to a faster cureing dynamics of clinical and laboratory manifestations of the disease.

scholarly journals Adolescent Nonalcoholic Fatty Liver Disease and Type 2 Diabetes in Young Adulthood

2020 ◽  
Vol 106 (1) ◽  
pp. e34-e44
Author(s):  
Aya Bardugo ◽  
Cole D Bendor ◽  
Inbar Zucker ◽  
Miri Lutski ◽  
Tali Cukierman-Yaffe ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Sensitivity Analyses ◽  
Control Group ◽  
Diabetes Incidence ◽  
Nonalcoholic Fatty Liver

Abstract Context The long-term risk of type 2 diabetes in adolescents with nonalcoholic fatty liver disease (NAFLD) is unclear. Objective To assess type 2 diabetes risk among adolescents with NAFLD. Design and Setting A nationwide, population-based study of Israeli adolescents who were examined before military service during 1997–2011 and were followed until December 31, 2016. Participants A total of 1 025 796 normoglycemic adolescents were included. Interventions Biopsy or radiographic tests were prerequisite for NAFLD diagnosis. Data were linked to the Israeli National Diabetes Registry. Main Outcome Measures Type 2 diabetes incidence. Results During a mean follow-up of 13.3 years, 12 of 633 adolescents with NAFLD (1.9%; all with high body mass index [BMI] at baseline) were diagnosed with type 2 diabetes compared with 2917 (0.3%) adolescents without NAFLD. The hazard ratio (HR) for type 2 diabetes was 2.59 (95% confidence interval [CI], 1.47–4.58) for the NAFLD vs. the non-NAFLD group after adjustment for BMI and sociodemographic confounders. The elevated risk persisted in several sensitivity analyses. These included an analysis of persons without other metabolic comorbidities (adjusted HR, 2.75 [95% CI, 1.48-5.14]) and of persons with high BMI; and an analysis whose outcome was type 2 diabetes by age 30 years (adjusted HR, 2.14 [95% CI, 1.02-4.52]). The results remained significant when a sex-, birth year-, and BMI-matched control group was the reference (adjusted HR, 2.98 [95% CI, 1.54-5.74]). Conclusions Among normoglycemic adolescents, NAFLD was associated with an increased adjusted risk for type 2 diabetes, which may be apparent before age 30 years.

Serum SHBG Is Associated With the Development and Regression of Nonalcoholic Fatty Liver Disease: A Prospective Study

2019 ◽  
Vol 105 (3) ◽  
pp. e791-e804
Author(s):  
Xu Wang ◽  
Jiewen Xie ◽  
Juan Pang ◽  
Hanyue Zhang ◽  
Xu Chen ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Prediction Models ◽  
Stepwise Logistic Regression ◽  
Stepwise Logistic Regression Analysis ◽  
Nonalcoholic Fatty Liver ◽  
Potential Biomarker

Abstract Context SHBG, a homodimeric glycoprotein produced by hepatocytes has been shown to be associated with metabolic disorders. Whether circulating SHBG levels are predictive of later risk of nonalcoholic fatty liver disease (NAFLD) remains unknown. In this study, we prospectively investigated the association between SHBG and NAFLD progression through a community-based cohort comprising 3389 Chinese adults. Methods NAFLD was diagnosed using abdominal ultrasonography. Serum SHBG levels were measured by chemiluminescent enzyme immunometric assay, and their relationship with NAFLD development and regression was investigated after a mean follow-up of 3.09 years using multivariable logistic regression. Results Basal SHBG was negatively associated with NAFLD development, with a fully adjusted odds ratio (OR) and its 95% confidence interval (CI) of 0.22 (0.12-0.40) (P &lt; .001). In contrast, basal SHBG was positively associated with NAFLD regression, with a fully adjusted OR of 4.83 (2.38-9.81) (P &lt; .001). Multiple-stepwise logistic regression analysis showed that SHBG concentration was an independent predictor of NAFLD development (OR, 0.28 [0.18-0.45]; P &lt; .001) and regression (OR, 3.89 [2.43-6.22]; P &lt; .001). In addition, the area under the receiver operating characteristic curves were 0.764 (95% CI, 0.740-0.787) and 0.762 (95% CI, 0.738-0.785) for the prediction models of NAFLD development and regression, respectively. Conclusions Serum SHBG concentration is associated with the development and regression of NAFLD; moreover, it can be a potential biomarker for predicting NAFLD progression, and also a novel preventive and therapeutic target for NAFLD.

scholarly journals Relationship Between Serum Uric Acid Levels and Nonalcoholic Fatty Liver Disease in Non-Obese Patients

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 600 ◽  
Author(s):  
Oral ◽  
Sahin ◽  
Turker ◽  
Kocak
Keyword(s):  
Uric Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Control Group ◽  
Nonalcoholic Fatty Liver ◽  
Non Invasive ◽  
Group I ◽  
The Relationship

Background and objectives: Nonalcoholic fatty liver disease (NAFLD) is associated with multiple factors such as hypertension, diabetes, dyslipidemia, obesity, and hyperuricemia. We aim to investigate the relationship between uric acid and NAFLD in a non-obese and young population. Materials and Methods: This study was performed in January 2010–2019 with a group of 367 (225 patients in the NAFLD group and 142 in the control group) patients with liver biopsy-proven NAFLD or no NAFLD. Patients with NAFLD were classified according to the percentage of steatosis as follows, group I had 1–20% and group II >20%. Demographic, clinical, and laboratory (biochemical parameters) features were collected retrospectively. Results: The mean body mass index (BMI) and age of the patients were 26.41 ± 3.42 and 32.27 ± 8.85, respectively. The BMI, homeostatic model of assessment (HOMA-IR), and uric acid (UA) values of the NAFLD group were found to be significantly higher than those of the controls. A positive correlation was found between the NAFLD stage and UA. The following factors were independently associated with NAFLD: BMI, HOMA-IR, and UA. In addition, the cut-off value of UA was 4.75 mg/dl with a sensitivity of 45.8% and a specificity of 80.3%. Conclusions: UA is a simple, non-invasive, cheap, and useful marker that may be used to predict steatosis in patients with NAFLD.

scholarly journals Exenatide Delays the Progression of Nonalcoholic Fatty Liver Disease in C57BL/6 Mice, Which May Involve Inhibition of the NLRP3 Inflammasome through the Mitophagy Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Shao ◽  
Xin-Yang Yu ◽  
Xue-Fei Ma ◽  
Wen-Jian Lin ◽  
Ming Hao ◽  
...  
Keyword(s):  
Body Weight ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Nlrp3 Inflammasome ◽  
Fatty Liver Disease ◽  
The Body ◽  
Control Group ◽  
Stress Injury ◽  
Nonalcoholic Fatty Liver

Objective. This study is aimed at investigating whether exenatide (Exe) delays the progression of nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice by targeting the NLRP3 inflammasome through the autophagy/mitophagy pathway. Methods. Thirty male C57BL/6 mice were randomly divided into three groups: control group (n=10), model group (n=10), and Exe (exenatide) group (n=10). Mouse models of NAFLD and diabetes were established using a high-fat diet and streptozocin. Results. The levels of fasting blood glucose (FBG), total cholesterol (TC), and triglyceride (TG) in the serum were significantly reduced after Exe treatment. The body weight, liver weight/body weight, and number of lipid droplets in the liver significantly decreased in Exe-treated mice. Treatment with Exe markedly reduced the levels of liver lipids, malondialdehyde (MDA), and alanine aminotransferase (ALT) in serum and livers. The number of autophagosomes increased significantly in the Exe group. The expression of LC3A/B-II/I, Beclin-1, Parkin, and BNIP3L increased significantly, whereas NLRP3 and IL-1β proteins were suppressed after Exe treatment. Conclusion. We successfully established a mouse model of NAFLD and diabetes. Exe may reduce oxidative stress injury and inhibit the NLRP3 inflammasome by enhancing the autophagy/mitophagy pathway in liver, which has a protective effect on the liver in NAFLD and diabetes in C57BL/6 mice.

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