scholarly journals Corrigendum to ‘The nonalcoholic fatty liver disease-like phenotype and lowered serum VLDL are associated with decreased expression and DNA hypermethylation of hepatic ApoB in male offspring of ApoE deficient mothers fed a with Western diet’ [Journal of Nutritional Biochemistry 77 (2020) 108319]

2021 ◽  
Vol 96 ◽  
pp. 108766
Author(s):  
Hsiao-Chien Chen ◽  
Yi-Zhen Chen ◽  
Chih-Hong Wang ◽  
Fu-Jung Lin
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Western Diet ◽  
Male Offspring ◽  
Dna Hypermethylation ◽  
Nonalcoholic Fatty Liver ◽  
Lowered Serum

scholarly journals Western diet induces nonalcoholic fatty liver disease and impairs liver mitochondrial metabolism in adult mice

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Patricia Pacheco ◽  
Vivian Santos ◽  
Fabiana Neves ◽  
Amelia Bernardo ◽  
Anatalia Vieira ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Western Diet ◽  
Mitochondrial Metabolism ◽  
Nonalcoholic Fatty Liver ◽  
Adult Mice

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.

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