scholarly journals Hyperferritinemia in patients with nonalcoholic fatty liver disease

2017 ◽  
Vol 63 (3) ◽  
pp. 284-289 ◽  
Author(s):  
Raffaelle K Barros ◽  
Helma Pinchemel Cotrim ◽  
Carla H Daltro ◽  
Yanaihara A Oliveira
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Diseases ◽  
Elevated Serum ◽  
Case Series ◽  
Clinical Approach ◽  
Retrospective Case ◽  
Nonalcoholic Fatty Liver

Summary Objective: In liver diseases, hyperferritinemia (HYF) is related to injured cells in acquired and genetic conditions with or without iron overload. It is frequent in patients with nonalcoholic fatty liver disease (NAFLD), in which it is necessary to define the mean of HYF to establish the better approach for them. The present study evaluated the significance of elevated ferritin in patients with NAFLD and steatohepatitis (NASH). Method: The review was performed using search instruments of indexed scientific material, including MEDLINE (by PubMed), Web of Science, IBECS and LILACS, to identify articles published in Portuguese, English and Spanish, from 2005 to May, 2016. Studies eligible included place and year of publication, diagnose criteria to NAFLD, specifications of serum ferritin measurements and/or liver histopathologic study. Exclusion criteria included studies with patients with alcohol consumption ≥ 20 g/day and other liver diseases. Results: A total of 11 from 30 articles were selected. It included 3,564 patients and they were cross-sectional, retrospective, case series and case-control. The result's analyses showed in 10 of these studies a relationship between ferritin elevated serum levels and NAFLD/NASH with and without fibrosis and insulin resistance. Conclusion: Hyperferritinemia in patients with NAFLD/NASH is associated more frequently with hepatocellular injury than hemochromatosis. These data suggest the relevance to evaluate carefully HYF in patients with NAFLD/NASH to establish appropriate clinical approach.

The Human Gut Microbiome in Liver Diseases

2017 ◽  
Vol 37 (02) ◽  
pp. 128-140 ◽  
Author(s):  
Brian Davis ◽  
Jasmohan Bajaj
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Primary Sclerosing Cholangitis ◽  
Alcoholic Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Diseases ◽  
Sclerosing Cholangitis ◽  
Nonalcoholic Fatty Liver

AbstractRecent advances in culture-independent laboratory techniques and bioinformatics have contributed to enriched characterizations of the gut microbiota and microbiome in chronic liver diseases such as alcoholic liver disease, nonalcoholic fatty liver disease, primary sclerosing cholangitis, primary biliary cholangitis, and cirrhosis. In this review, the authors focus on studies characterizing and modulating the gut microbiota and microbiome in humans. The majority of studies that characterized microbiota involved a small number of patients using 16S ribosomal RNA genetic sequencing. Few studies applied whole-genome shotgun sequencing and metagenomics analyses. The majority of clinical trials on modulating the microbiome have focused on probiotics or antibiotics in small groups of patients with cirrhosis versus healthy controls. Several trials are underway using fecal microbial transplantation in alcoholic liver disease, nonalcoholic fatty liver disease, primary sclerosing cholangitis, and cirrhosis. Future research is needed on understanding the viral and fungal microbiome and developing user-friendly microbiome tools.

scholarly journals Cisd2 Protects the Liver from Oxidative Stress and Ameliorates Western Diet-Induced Nonalcoholic Fatty Liver Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 559
Author(s):  
Yi-Long Huang ◽  
Zhao-Qing Shen ◽  
Chen-Hua Huang ◽  
Yuan-Chi Teng ◽  
Chao-Hsiung Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Diseases ◽  
Cholesterol Biosynthesis ◽  
Severe Form ◽  
Western Diet ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) and its more severe form, nonalcoholic steatohepatitis (NASH), are the most common chronic liver diseases worldwide. However, drugs to treat NAFLD and NASH are an unmet clinical need. This study sought to provide evidence that Cisd2 is a molecular target for the development of treatments targeting NAFLD and NASH. Several discoveries are pinpointed. The first is that Cisd2 dosage modulates the severity of Western diet-induced (WD-induced) NAFLD. Specifically, Cisd2 haploinsufficiency accelerates NAFLD development and exacerbates progression toward NASH. Conversely, an enhanced Cisd2 copy number attenuates liver pathogenesis. Secondly, when a WD is fed to mice, transcriptomic analysis reveals that the major alterations affecting biological processes are related to inflammation, lipid metabolism, and DNA replication/repair. Thirdly, among these differentially expressed genes, the most significant changes involve Nrf2-mediated oxidative stress, cholesterol biosynthesis, and fatty acid metabolism. Finally, increased Cisd2 expression protects the liver from oxidative stress and reduces the occurrence of mitochondrial DNA deletions. Taken together, our mouse model reveals that Cisd2 plays a crucial role in protecting the liver from WD-induced damages. The development of therapeutic agents that effectively enhance Cisd2 expression is one potential approach to the treatment of WD-induced fatty liver diseases.

scholarly journals Nonalcoholic Fatty Liver Disease: A Clinical Approach and Review

2006 ◽  
Vol 20 (5) ◽  
pp. 345-349 ◽  
Author(s):  
Maitreyi Raman ◽  
Johane Allard
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Clinical Approach ◽  
Pharmacological Agents ◽  
Nonalcoholic Fatty Liver ◽  
Alcoholic Steatohepatitis ◽  
Obesity And Diabetes ◽  
Include Body Mass Index

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of incidental elevation of liver enzymes in North America and Europe. Risk factors for NAFLD include body mass index of 25 kg/m2or greater, central obesity and diabetes mellitus. The spectrum of disease is variable, ranging from simple steatosis with benign prognosis, to non-alcoholic steatohepatitis and cirrhosis, conferring increase in morbidity and mortality. The primary abnormality or ‘first hit’ in patients with NAFLD is insulin resistance leading to hepatic steatosis. The second hit involves multiple proinflammatory cytokines resulting in non-alcoholic steatohepatitis. Treatment is aimed at aggressive risk factor control and weight loss. Currently, there are no pharmacological agents recommended in the treatment of NAFLD, although preliminary studies suggest promising agents in the future.

scholarly journals Presumed Nonalcoholic Fatty Liver Disease Among Medicare Beneficiaries With HIV, 2006–2016

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
James M Paik ◽  
Linda Henry ◽  
Pegah Golabi ◽  
Saleh A Alqahtani ◽  
Gregory Trimble ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Diseases ◽  
Medicare Beneficiaries ◽  
Hiv Patients ◽  
Annual Percent Change ◽  
Cross Sectional ◽  
Nonalcoholic Fatty Liver

Abstract Background Newer treatments for HIV and hepatitis C virus (HCV) have decreased mortality in HIV/HCV patients. Nonalcoholic fatty liver disease (NAFLD) has increased globally; therefore, the prevalence and mortality of NAFLD among HIV (+) patients was assessed. Methods Using Medicare denominator, inpatient, and outpatient files (random 5% sample per year), serial cross-sectional analysis (2006 to 2016) was performed. Joinpoint trend analysis evaluated prevalence and mortality with average annual percent change (AAPC). HIV (+) patients and liver diseases (LDs) were identified using International Classification of Diseases 9/10 codes. NAFLD was presumed using diagnosis codes or codes for metabolic dysfunction and obesity in absence of other LDs. Liver-related HIV (+) indicated HIV (+) patients with LDs. Results Among 28 675 887 Medicare beneficiaries, 47 062 were HIV (+) (mean [SD] age, 51.4 [11.3] years); 11 920 had liver diseases (6923 HCV, 2019 hepatitis B virus [HBV], 2472 presumed NAFLD, 278 alcoholic liver disease [ALD], and 1653 other LDs); 2882 HIV (+) patients died; 1260 had LDs. The prevalence and mortality for non-liver-related HIV (+) decreased (AAPC, –1.1% and –9.1%). Liver-related HIV (+) increased (AAPC, 1.7%; P = .007); mortality leveled off. Prevalence and mortality worsened for presumed NAFLD (AAPC, 9.7% and 10.0%) and improved for HBV and HCV (HBV: AAPC, –3.5% and –8.8%; HCV: AAPC, –0.7% and –4.9%). After adjustments, HCV (odds ratio [OR], 2.00; 95% confidence interval [CI], 1.24–172), HBV (OR, 2.40; 95% CI, 2.09–2.77), ALD (OR, 5.70; 95% CI, 4.34–7.48), and presumed NAFLD (OR, 1.46; 95% CI, 1.24–1.72) increased 1-year mortality. Conclusions Among HIV (+) subjects, viral hepatitis remains the leading LD for increased 1-year mortality, but the prevalence and mortality with presumed NAFLD are increasing.

scholarly journals Antiresistin RNA Oligonucleotide Ameliorates Diet-Induced Nonalcoholic Fatty Liver Disease in Mice through Attenuating Proinflammatory Cytokines

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Yi Tan ◽  
Xing Liang Jin ◽  
Weiguo Lao ◽  
Jane Kim ◽  
Linda Xiao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Proinflammatory Cytokines ◽  
Fatty Liver Disease ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Regulatory Element ◽  
Elevated Serum ◽  
Tolerance Test ◽  
Nonalcoholic Fatty Liver

The aim of this study was to determine whether inhibition of resistin by a synthetic antiresistin RNA (oligonucleotide) oligo ameliorates metabolic and histological abnormalities in nonalcoholic fatty liver disease (NAFLD) induced by high-fat diet (HFD) in mice. The antiresistin RNA oligo and a scrambled control oligo (25 mg/kg of body weight) were i.p. injected to HFD mice. Serum metabolic parameters and hepatic enzymes were measured after 4-week treatment. The treatment significantly reduced epididymal fat and attenuated the elevated serum resistin, cholesterol, triglycerides, glucose, and insulin with an improved glucose tolerance test. Antiresistin RNA oligo also normalized serum AST and ALT levels with improved pathohistology of NAFLD. Immunoblotting and qRT-PCR revealed that decreased protein and mRNA expression of resistin in fat and liver tissues of the treated mice were associated with reduction of adipose TNF-αand IL-6 expression and secretion into circulation. mRNA and protein expression of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and sterol regulatory element-binding protein-1c (SREBP-1c) were also significantly decreased in the treated mice. Our results suggest that resistin may exacerbate NAFLD in metabolic syndrome through upregulating inflammatory cytokines and hepatic PEPCK and SREBP-1c. Antiresistin RNA oligo ameliorated metabolic abnormalities and histopathology of NAFLD through attenuating proinflammatory cytokines.

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