Murine models provide insight to the development of non-alcoholic fatty liver disease
Open accessAbstract
Associated with the obesity epidemic, non-alcoholic fatty liver disease (NAFLD) has become the leading liver disease in North America. Approximately 30 % of patients with NAFLD may develop non-alcoholic steatohepatitis (NASH) that can lead to cirrhosis and hepatocellular carcinoma (HCC). Frequently animal models are used to help identify underlying factors contributing to NAFLD including insulin resistance, dysregulated lipid metabolism and mitochondrial stress. However, studying the inflammatory, progressive nature of NASH in the context of obesity has proven to be a challenge in mice. Although the development of effective treatment strategies for NAFLD and NASH is gaining momentum, the field is hindered by a lack of a concise animal model that reflects the development of liver disease during obesity and the metabolic syndrome. Therefore, selecting an animal model to study NAFLD or NASH must be done carefully to ensure the optimal application. The most widely used animal models have been reviewed highlighting their advantages and disadvantages to studying NAFLD and NASH specifically in the context of obesity.
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The standard HFD induces insulin resistance systemically and in the liver but does not induce NASH.
“utilizing the standard HFD that induces insulin resistance systemically and in the liver 60 but does not induce NASH 61”
From Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis (2024) · cites this paper as [61]
The High-cholesterol and -cholic acid diets section reports that HFD alone did not produce steatohepatitis in a 30-week comparison, supporting the citation’s point under that condition. But the High-fat diets and Extended duration of high-fat diets sections describe NASH-like inflammation and less severe NASH after longer HFD feeding, so the unqualified claim that a standard HFD does not induce NASH overstates the source. The sentence attaches this citation to the NASH claim, not the insulin-resistance claim. (LLM, conf=0.86)
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References 97 · Cited by 26
Research works printed but not linked: 1
- Podrini C, Cambridge EL, Lelliott CJ, et al. (2013) High-fat feeding rapidly induces obesity and lipid derangements in C57BL/6N mice. Mamm Genome 24, 240-251.
- Authors
- Reid, D. T., & Eksteen, B.
- Affiliations
- University of Calgary (CA)
- Corresponding author
- Eksteen, B.
- ORCID
- Eksteen, B.
- Venue
- Nutrition Research Reviews
- Publisher
- Cambridge University Press (CUP)
- Published
- 2015-10-23
- Volume
- 28
- Issue
- 2
- Pages
- 133-142
- ISSN
- 0954-4224 (ISSN-L)
- 1475-2700
- OpenAlex
- W2177414021
- Cited by
- 26
- References
- 97
- Citations by year
- 2024: 5 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 4
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nutrition Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, obesity, metabolic syndrome, insulin resistance, lipid metabolism, mitochondrial stress, liver inflammation, hepatocellular carcinoma, liver cirrhosis
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