scholarly journals Nutritive Value and Quality of Sweet Basil Leaves in an Animal Model of Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Samah El-Hashash
2019 ◽  
Vol 170 (2) ◽  
pp. 273-282 ◽  
Author(s):  
Barbara Borowa-Mazgaj ◽  
Aline de Conti ◽  
Volodymyr Tryndyak ◽  
Colleen R Steward ◽  
Leandro Jimenez ◽  
...  

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.


Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1439
Author(s):  
Guglielmina Chimienti ◽  
Antonella Orlando ◽  
Francesco Russo ◽  
Benedetta D’Attoma ◽  
Manuela Aragno ◽  
...  

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.


HORMONES ◽  
2021 ◽  
Author(s):  
Ilias Vachliotis ◽  
Antonis Goulas ◽  
Paraskevi Papaioannidou ◽  
Stergios A. Polyzos

2016 ◽  
Vol 9 (4) ◽  
pp. 463-472 ◽  
Author(s):  
David Briskey ◽  
Mandy Heritage ◽  
Lesley-Anne Jaskowski ◽  
Jonathan Peake ◽  
Glenda Gobe ◽  
...  

2021 ◽  
Author(s):  
Xianhao Yi ◽  
Shaihong Zhu ◽  
Liyong Zhu

Abstract Background: Many studies have shown that visceral adiposity index (VAI) is valuable in the diagnosis of nonalcoholic fatty liver disease (NAFLD), but the accuracy of VAI in the diagnosis of NAFLD is not consistent. we aimed to assess the VAI as a predictor of NAFLD. Methods: The Cochrane Library, PubMed, Embase, and other databases were searched to collect all the documents that meet the inclusion criteria, The retrieval period is from the establishment of the database to September 2021. The methodological quality of the included studies was evaluated using the quadas-2 tool. The heterogeneity among the studies was analyzed by the Cochran-Q test and I2 test, and the appropriate model was selected according to the heterogeneity. The diagnostic efficacy of VAI was evaluated by meta-analysis and a Fagan diagram was drawn to evaluate the diagnostic ability of VAI.Results: A total of 9 studies were included. The overall quality of the included studies was good. Meta-analysis showed that the combined sensitivity (Sen combined) of VAI in the diagnosis of NAFLD was 0.70 [95% CI (0.69-0.71)], the combined specificity (Spe combined) was 0.67 [95% CI (0.67-0.68)], PLR combined was 2.08 [95% CI (1.87-2.31)], NLP combined was 0.39 [95% CI (0.34-0.44)], and DOR combined was 5.81 [95% CI (4.73-7.14)]. The corresponding AUC was 0.79 [95% CI (0.75-0.82)]. Meta-regression analysis showed that the gold index was a potential source of heterogeneity (P < 0.05). The Fagan diagram shows that the precision of NAFLD diagnosis is 70% when the pre-test probability is set to 50% and then supplemented by VAI.Conclusion: VAI has a certain value in the diagnosis of NAFLD and may be helpful in the early detection of NAFLD, but it still needed a large number of prospective studies to support this.


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