ArticleAlcoholism, clinical and experimental research2014
Modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protects against alcoholic liver disease.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 68 citations in OpenAlex.
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- Pathogenesis of Alcohol-Associated Fatty Liver: Lessons From Transgenic Mice.Frontiers in physiology · 2022Review
- Alcohol and Metabolic-associated Fatty Liver Disease.Journal of clinical and translational hepatology · 2021Review
- Alcohol's Impact on the Gut and Liver.Nutrients · 2021Review
- Ahnak deficiency attenuates high-fat diet-induced fatty liver in mice through FGF21 induction.Experimental & molecular medicine · 2021Article
- Alcoholic hepatitis and metabolic disturbance in female mice: a more tractable model thanDisease models & mechanisms · 2020Article
- Gypenosides Protect Orbital Fibroblasts in Graves Ophthalmopathy via Anti-Inflammation and Anti-Fibrosis Effects.Investigative ophthalmology & visual science · 2020Article
- Metabolomic alterations associated with Kallmann syndrome.Annals of translational medicine · 2020Article
- [Diagnosis and treatment strategies for fatty liver when obesity coexists with alcohol consumption].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- Mesenchymal stem cells alleviate liver injury induced by chronic-binge ethanol feeding in mice via release of TSG6 and suppression of STAT3 activation.Stem cell research & therapy · 2020Article
- Pathogenesis and pathways: nonalcoholic fatty liver disease & alcoholic liver disease.Translational gastroenterology and hepatology · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic alcohol intake affects liver function and causes hepatic pathological changes. It has been shown that peroxisome proliferator-activated receptor α (PPARα)-null mice developed more pronounced hepatic changes than wild-type (WT) mice after chronic exposure to a diet containing 4% alcohol. The remarkable similarity between the histopathology of alcoholic liver disease (ALD) in Ppara-null model and in humans, and the fact that PPARα expression and activity in human liver are less than one-tenth of those in WT mouse liver make Ppara-null a good system to investigate ALD.
methodsIn this study, the Ppara-null model was used to elucidate the dynamic regulation of PPARα activity during chronic alcohol intake. Hepatic transcriptomic and metabolomic analyses were used to examine alterations of gene expression and metabolites associated with pathological changes. The changes triggered by alcohol consumption on gene expression and metabolites in Ppara-null mice were compared with those in WT mice.
resultsThe results showed that in the presence of PPARα, 3 major metabolic pathways in mitochondria, namely the fatty acid β-oxidation, the tricarboxylic acid cycle, and the electron transfer chain, were induced in response to a 2-month alcohol feeding, while these responses were greatly reduced in the absence of PPARα. In line with the transcriptional modulations of these metabolic pathways, a progressive accumulation of triglycerides, a robust increase in hepatic cholic acid and its derivatives, and a strong induction of fibrogenesis genes were observed exclusively in alcohol-fed Ppara-null mice.
conclusionsThese observations indicate that PPARα plays a protective role to enhance mitochondrial function in response to chronic alcohol consumption by adaptive transcriptional activation and suggest that activation of this nuclear receptor may be of therapeutic value in the treatment for ALD.
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