ArticleGastroenterology2015
Fat-Specific Protein 27/CIDEC Promotes Development of Alcoholic Steatohepatitis in Mice and Humans.
Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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85 citing papers in PubMed, 140 citations in OpenAlex.
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- An Update on Animal Models of Alcohol-Associated Liver Disease.The American journal of pathology · 2026Review
- CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of mitochondria-associated hub genes related to alcohol-associated liver fibrosis progression in aldehyde dehydrogenase 2 deficiency.Frontiers in physiology · 2026Article
- Perfluorooctane sulfonate exposure and alcohol-associated liver disease severity in a mouse chronic-binge ethanol feeding model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
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- FABP4 deficiency ameliorates alcoholic steatohepatitis in mice via inhibition of p53 signaling pathway.Scientific reports · 2024Article
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- Pregnane X receptor knockout mitigates weight gain and hepatic metabolic dysregulation in female C57BL/6 J mice on a long-term high-fat diet.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
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- Alcohol-associated liver disease.The Journal of clinical investigation · 2024Review
- Alcohol-related liver disease (ALD): current perspectives on pathogenesis, therapeutic strategies, and animal models.Frontiers in pharmacology · 2024Review
- Evaluation of vital genes correlated with CD8 + T cell infiltration as prognostic biomarkers in stomach adenocarcinoma.BMC gastroenterology · 2023Article
- Nuclear miR-150 enhances hepatic lipid accumulation by targeting RNA transcripts overlapping theiScience · 2023Article
- Deficiency of gluconeogenic enzyme PCK1 promotes metabolic-associated fatty liver disease through PI3K/AKT/PDGF axis activation in male mice.Nature communications · 2023Article
- The Emerging Role of Ferroptosis in Various Chronic Liver Diseases: Opportunity or Challenge.Journal of inflammation research · 2023Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 9 institutions in 4 countries.
Funding
Abstract
BACKGROUND &
aimsAlcoholic steatohepatitis (ASH) is the progressive form of alcoholic liver disease and may lead to cirrhosis and hepatocellular carcinoma. We studied mouse models and human tissues to identify molecules associated with ASH progression and focused on the mouse fat-specific protein 27 (FSP-27)/human cell death-inducing DFF45-like effector C (CIDEC) protein, which is expressed in white adipose tissues and promotes formation of fat droplets.
methodsC57BL/6N mice or mice with hepatocyte-specific disruption of Fsp27 (Fsp27(Hep-/-) mice) were fed the Lieber-Decarli ethanol liquid diet (5% ethanol) for 10 days to 12 weeks, followed by 1 or multiple binges of ethanol (5 or 6 g/kg) during the chronic feeding. Some mice were given an inhibitor (GW9662) of peroxisome proliferator-activated receptor γ (PPARG). Adenoviral vectors were used to express transgenes or small hairpin (sh) RNAs in cultured hepatocytes and in mice. Liver tissue samples were collected from ethanol-fed mice or from 31 patients with alcoholic hepatitis (AH) with biopsy-proved ASH and analyzed histologically and immunohistochemically and by transcriptome, immunoblotting, and real-time PCR analyses.
resultsChronic-plus-binge ethanol feeding of mice, which mimics the drinking pattern of patients with AH, produced severe ASH and mild fibrosis. Microarray analyses revealed similar alterations in expression of many hepatic genes in ethanol-fed mice and humans with ASH, including up-regulation of mouse Fsp27 (also called Cidec) and human CIDEC. Fsp27(Hep-/-) mice and mice given injections of adenovirus-Fsp27shRNA had markedly reduced ASH following chronic-plus-binge ethanol feeding. Inhibition of PPARG and cyclic AMP-responsive element binding protein H (CREBH) prevented the increases in Fsp27α and FSP27β mRNAs, respectively, and reduced liver injury in this chronic-plus-binge ethanol feeding model. Overexpression of FSP27 and ethanol exposure had synergistic effects in inducing production of mitochondrial reactive oxygen species and damage to hepatocytes in mice. Hepatic CIDEC mRNA expression was increased in patients with AH and correlated with the degree of hepatic steatosis and disease severity including mortality.
conclusionsIn mice, chronic-plus-binge ethanol feeding induces ASH that mimics some histological and molecular features observed in patients with AH. Hepatic expression of FSP27/CIDEC is highly up-regulated in mice following chronic-plus-binge ethanol feeding and in patients with AH; this up-regulation contributes to alcohol-induced liver damage.
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