Male LEW.1WR1 Rats Develop Metabolic Dysfunction, Steatohepatitis, and Liver Damage

Most patients with non-alcoholic steatohepatitis (NASH) have insulin resistance, and there is a near-universal association between NASH and insulin resistance. Insulin resistance induces lipid accumulation in the liver, leading to the development of metabolic syndrome. However, most NASH rodent mode...

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Published inEndocrines Vol. 5; no. 2; pp. 166 - 185
Main Authors Wilkerson-Vidal, Quiana C., Wimalarathne, Madushika M., Hunt, Emily C., Mercado, Luis, David, Moses Adaji, Apperson, Christopher R., Smiley, Alan, Love-Rutledge, Sharifa Tahirah, Vogler, Bernhard W. G.
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 19.04.2024
Subjects
Animals
Diabetes
Diet
fibrosis
Glucose
hyperinsulinemia
Inflammation
Insulin resistance
Lipids
Liver diseases
Metabolic disorders
metabolomics
nonalcoholic fatty liver
nonalcoholic steatohepatitis
obesity
Pathogenesis
United States > US
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Summary:Most patients with non-alcoholic steatohepatitis (NASH) have insulin resistance, and there is a near-universal association between NASH and insulin resistance. Insulin resistance induces lipid accumulation in the liver, leading to the development of metabolic syndrome. However, most NASH rodent models fail to develop metabolic syndrome. LEW.1WR1 rats that are 23 weeks old showed increased body mass, epididymal fat, and liver mass, suggesting obesity-driven metabolic dysfunction. We have characterized steatosis, inflammation, Mallory–Denk body formation with hematoxylin and eosin (H&E), and fibrosis with Trichome blue staining. The presence of hepatic fibrosis with other features of NASH described above is one of the major strengths of this model since most of the currently available NASH models do not develop microvesicular steatosis or fibrosis. Together with the other important features of NASH described above, we confirm that male LEW.1WR1 rats develop NASH and insulin resistance with a standard diet.
ISSN:2673-396X
2673-396X
DOI:10.3390/endocrines5020012