ArticleDisease models & mechanisms2015
A modified choline-deficient, ethionine-supplemented diet reduces morbidity and retains a liver progenitor cell response in mice.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing.Cell research · 2023Article
- Experimental Models for Studying Structural and Functional State of the Pathological Liver (Review).Sovremennye tekhnologii v meditsine · 2023Review
- Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research.International journal of molecular sciences · 2022Review
- Article
- Addressing the liver progenitor cell response and hepatic oxidative stress in experimental non-alcoholic fatty liver disease/non-alcoholic steatohepatitis using amniotic epithelial cells.Stem cell research & therapy · 2021Article
- All routes lead to Rome: multifaceted origin of hepatocytes during liver regeneration.Cell regeneration (London, England) · 2021Review
- In Vitro and In Vivo Models of Non-Alcoholic Fatty Liver Disease: A Critical Appraisal.Journal of clinical medicine · 2020Review
- Founder cells for hepatocytes during liver regeneration: from identification to application.Cellular and molecular life sciences : CMLS · 2020Review
- Loss of ARF/INK4A Promotes Liver Progenitor Cell Transformation Toward Tumorigenicity Supporting Their Role in Hepatocarcinogenesis.Gene expression · 2020Article
- Cholecystokinin Receptor Antagonist Therapy Decreases Inflammation and Fibrosis in Chronic Pancreatitis.Digestive diseases and sciences · 2020Article
- Cellular and molecular basis of liver regeneration.Seminars in cell & developmental biology · 2020Review
- A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma.Digestive diseases and sciences · 2020Article
- Hepatic progenitor cell activation is induced by the depletion of the gut microbiome in mice.MicrobiologyOpen · 2019Article
- Autophagy promotes hepatic differentiation of hepatic progenitor cells by regulating the Wnt/β-catenin signaling pathway.Journal of molecular histology · 2019Article
- Human Amnion Epithelial Cell Therapy for Chronic Liver Disease.Stem cells international · 2019Review
- InForm software: a semi-automated research tool to identify presumptive human hepatic progenitor cells, and other histological features of pathological significance.Scientific reports · 2018Article
- Apoptosis in the aging liver.Oncotarget · 2017Review
- Pigment epithelium-derived factor (PEDF) peptide promotes the expansion of hepatic stem/progenitor cells via ERK and STAT3-dependent signaling.American journal of translational research · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The choline-deficient, ethionine-supplemented (CDE) dietary model induces chronic liver damage, and stimulates liver progenitor cell (LPC)-mediated repair. Long-term CDE administration leads to hepatocellular carcinoma in rodents and lineage-tracing studies show that LPCs differentiate into functional hepatocytes in this model. The CDE diet was first modified for mice by our laboratory by separately administering choline-deficient chow and ethionine in the drinking water (CD+E diet). Although this CD+E diet is widely used, concerns with variability in weight loss, morbidity, mortality and LPC response have been raised by researchers who have adopted this model. We propose that these inconsistencies are due to differential consumption of chow and ethionine in the drinking water, and that incorporating ethionine in the choline-deficient chow, and altering the strength, will achieve better outcomes. Therefore, C57Bl/6 mice, 5 and 6 weeks of age, were fed an all-inclusive CDE diet of various strengths (67% to 100%) for 3 weeks. The LPC response was quantitated and cell lines were derived. We found that animal survival, LPC response and liver damage are correlated with CDE diet strength. The 67% and 75% CDE diet administered to mice older than 5 weeks and greater than 18 g provides a consistent and acceptable level of animal welfare and induces a substantial LPC response, permitting their isolation and establishment of cell lines. This study shows that an all-inclusive CDE diet for mice reproducibly induces an LPC response conducive to in vivo studies and isolation, whilst minimizing morbidity and mortality.
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