ArticleFEBS open bio2021
Nonobese mice with nonalcoholic steatohepatitis fed on a choline-deficient, l-amino acid-defined, high-fat diet exhibit alterations in signaling pathways.
Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Susceptibility and transcriptional characteristics of inbred C57BL/6J and outbred ICR mice in CDAHFD-induced MASH models.Laboratory animal research · 2026Article
- CBP/β-Catenin Signaling in Hepatocytes Plays Pivotal Roles in MMP-7-Mediated Liver Fibrosis in a Metabolic Dysfunction-Associated Steatohepatitis Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Roles of mitochondrial complexes in non-alcoholic fatty liver disease.Frontiers in molecular biosciences · 2026Review
- Era of metabolic dysfunction-associated steatotic liver disease and impact on the liver donor pool.World journal of gastroenterology · 2025Review
- Review
- Mouse models of nonalcoholic fatty liver disease (NAFLD): pathomechanisms and pharmacotherapies.International journal of biological sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
Nonalcoholic steatohepatitis (NASH) is often associated with obesity, but some patients develop NASH without obesity. The physiological processes by which nonobese patients develop NASH and cirrhosis have not yet been determined. Here, we analyzed the effects of dietary methionine content on NASH induced in mice fed on a choline-deficient, methionine-lowered, l-amino acid-defined high-fat diet (CDAHFD). CDAHFD with insufficient methionine induced insulin sensitivity and enhanced NASH pathology, but without obesity. In contrast, CDAHFD with sufficient methionine induced steatosis, and unlike CDAHFD with insufficient methionine, also induced obesity and insulin resistance. Gene profile analysis revealed that the disease severity in CDAHFD may partially be due to upregulation of the Rho family GTPases pathway and mitochondrial and nuclear receptor signal dysfunction. The signaling factors/pathways detected in this study may assist in future study of NASH regulation, especially its 'nonobese' subtype.
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