scholarly journals Hepatoprotective Effects of Insect Extracts in an Animal Model of Nonalcoholic Fatty Liver Disease

Nutrients ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 735 ◽  
Author(s):  
A-Rang Im ◽  
Won-Kyung Yang ◽  
Yang-Chun Park ◽  
Seung Kim ◽  
Sungwook Chae
Keyword(s):  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects

scholarly journals Gene Expression and DNA Methylation Alterations in the Glycine N-Methyltransferase Gene in Diet-Induced Nonalcoholic Fatty Liver Disease-Associated Carcinogenesis

2019 ◽  
Vol 170 (2) ◽  
pp. 273-282 ◽  
Author(s):  
Barbara Borowa-Mazgaj ◽  
Aline de Conti ◽  
Volodymyr Tryndyak ◽  
Colleen R Steward ◽  
Leandro Jimenez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
The United States ◽  
Down Regulation ◽  
Nonalcoholic Fatty Liver

Abstract Nonalcoholic fatty liver disease (NAFLD) is becoming a major etiological risk factor for hepatocellular carcinoma (HCC) in the United States and other Western countries. In this study, we investigated the role of gene-specific promoter cytosine DNA methylation and gene expression alterations in the development of NAFLD-associated HCC in mice using (1) a diet-induced animal model of NAFLD, (2) a Stelic Animal Model of nonalcoholic steatohepatitis-derived HCC, and (3) a choline- and folate-deficient (CFD) diet (CFD model). We found that the development of NAFLD and its progression to HCC was characterized by down-regulation of glycine N-methyltransferase (Gnmt) and this was mediated by progressive Gnmt promoter cytosine DNA hypermethylation. Using a panel of genetically diverse inbred mice, we observed that Gnmt down-regulation was an early event in the pathogenesis of NAFLD and correlated with the extent of the NAFLD-like liver injury. Reduced GNMT expression was also found in human HCC tissue and liver cancer cell lines. In in vitro experiments, we demonstrated that one of the consequences of GNMT inhibition was an increase in genome methylation facilitated by an elevated level of S-adenosyl-L-methionine. Overall, our findings suggest that reduced Gnmt expression caused by promoter hypermethylation is one of the key molecular events in the development of NAFLD-derived HCC and that assessing Gnmt methylation level may be useful for disease stratification.

scholarly journals Hepatoprotective Effects of a Novel Trihoney against Nonalcoholic Fatty Liver Disease: A Comparative Study with Atorvastatin

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Hamad Abdulsalam Hamad Alfarisi ◽  
Muhammad Bin Ibrahim ◽  
Zenab B. Hamad Mohamed ◽  
Nuraniza Azahari ◽  
Asmah Hanim Bt. Hamdan ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Function ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Normal Diet ◽  
Cholesterol Diet ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects ◽  
Glutamyl Transferase

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder worldwide with no curative therapy. The aim of this study was to investigate the hepatoprotective effects of a novel Trihoney against biochemical and histological manifestations of NAFLD in hypercholesterolemic rabbits. Methodology. Forty-eight male New Zealand white (NZW) rabbits were grouped into normal diet (C), normal diet with 0.6 g/kg/day of Trihoney (C + H), 1% cholesterol diet (HCD), 1% cholesterol diet with 0.3 g/kg/day of Trihoney (HCD + H1), 1% cholesterol diet with 0.6 g/kg/day of Trihoney (HCD + H2), and 1% cholesterol diet with 2 mg/kg/day of atorvastatin (HCD + At.). Animals were sacrificed after 12 weeks of treatment. Serum lipids and liver function test (LFT) were measured prior to and at the endpoint of the experiment for total cholesterol (TC), low-density lipoprotein (LDL-c), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and total bilirubin (T. Bil.). Liver was processed for histopathology study. Liver homogenate was analysed for oxidative stress parameters: superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA). Results. Lipid analysis approved the induction of hypercholesterolemia. A significant elevation (p<0.01) of serum AST and ALT levels showed by the HCD group was compared to C and C + H groups. Trihoney exhibited a significant reduction (p<0.001) of AST and ALT compared to the HCD group. Likewise, AST and ALT reduced significantly in the HCD + At. group (p<0.001). Trihoney supplementation induced significant (p<0.05) enhancement of SOD and GPx activities. Atorvastatin treatment was associated with significant (p<0.05) reduction of SOD and GPx activities in the liver. Trihoney and atorvastatin showed marked (p<0.001) reduction of hepatic lipid peroxidation. Trihoney showed histological protection against progression of NAFLD to nonalcoholic steatohepatitis (NASH). Atorvastatin exhibited no beneficial impact on hepatic architecture. Conclusion. Trihoney was able to maintain normal liver function and showed hepatoprotection against progression of NAFLD to NASH probably through hypocholesterolaemic and antioxidant functions.

scholarly journals The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease

Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1439
Author(s):  
Guglielmina Chimienti ◽  
Antonella Orlando ◽  
Francesco Russo ◽  
Benedetta D’Attoma ◽  
Manuela Aragno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Mitochondrial Oxidative Stress ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence and effects of mitochondrial oxidative stress in the liver from rats fed a high-fat plus fructose (HF-F) diet inducing NAFLD. Supplementation with dehydroepiandrosterone (DHEA), a multitarget antioxidant, was tested for efficacy in delaying NAFLD. A marked mitochondrial oxidative stress was originated by all diets, as demonstrated by the decrease in Superoxide Dismutase 2 (SOD2) and Peroxiredoxin III (PrxIII) amounts. All diets induced a decrease in mitochondrial DNA content and an increase in its oxidative damage. The diets negatively affected mitochondrial biogenesis as shown by decreased peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), mitochondrial transcription factor A (TFAM), and the COX-IV subunit from the cytochrome c oxidase complex. The reduced amounts of Beclin-1 and lipidated LC3 II form of the microtubule-associated protein 1 light chain 3 (LC3) unveiled the diet-related autophagy’s decrease. The DHEA supplementation did not prevent the diet-induced changes. These results demonstrate the relevance of mitochondrial oxidative stress and the sequential dysfunction of the organelles in an obesogenic diet animal model of NAFLD.

scholarly journals Probiotics modify tight-junction proteins in an animal model of nonalcoholic fatty liver disease

2016 ◽  
Vol 9 (4) ◽  
pp. 463-472 ◽  
Author(s):  
David Briskey ◽  
Mandy Heritage ◽  
Lesley-Anne Jaskowski ◽  
Jonathan Peake ◽  
Glenda Gobe ◽  
...  
Keyword(s):  
Animal Model ◽  
Liver Disease ◽  
Tight Junction ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Tight Junction Proteins ◽  
Nonalcoholic Fatty Liver ◽  
Junction Proteins

scholarly journals Diet switch and omega-3 hydroxy-fatty acids display differential hepatoprotective effects in an obesity/nonalcoholic fatty liver disease model in mice

2018 ◽  
Vol 24 (4) ◽  
pp. 461-474 ◽  
Author(s):  
Roberto Rodriguez-Echevarria ◽  
Jose Macias-Barragan ◽  
Marcela Parra-Vargas ◽  
Judith Rebeca Davila-Rodriguez ◽  
Eduardo Amezcua-Galvez ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Disease Model ◽  
Omega 3 ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects ◽  
Diet Switch

Bioinformatics analysis of an animal model of diet-induced nonalcoholic fatty liver disease with rapid progression

2021 ◽  
pp. 153537022110550
Author(s):  
Wei Hong ◽  
Tingting Zhang ◽  
Junbin Yan ◽  
Jianshun Yu ◽  
Beihui He ◽  
...  
Keyword(s):  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Mongolian Gerbil ◽  
Fatty Liver Disease ◽  
Bioinformatics Analysis ◽  
Rapid Progression ◽  
Mongolian Gerbils ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) develops rapidly in high-fat diet (HFD) fed Mongolian gerbil ( Meriones unguiculatus). Here, we aim to explore the gene expression characteristics of Mongolian gerbil to better understand the underlying mechanism in this animal model. Mongolian gerbils were fed with normal diet or HFD for different periods. High-throughput sequencing was carried out on the hepatic mRNA and bioinformatics analysis was further performed. Eight hub genes Cd44, App, Cdc42, Cd68, Cxcr4, Csf1r, Adgre1, and Fermt3, which were involved in inflammation, fibrosis, and HCC were obtained. Four significant independent poor prognostic factors for HCC (GPC1, ARPC1B, DAB2, and CFL1) were screened out. qRT-PCR result showed that the above genes expressed high levels in different periods of modeling process. The findings of this study provide useful information for further studies on Mongolian gerbil NAFLD model.

Sign in / Sign up

Export Citation Format

Share Document