A simple method for inducing nonalcoholic steatohepatitis with fibrosis

Background Nonalcoholic fatty liver disease (NAFLD) is increasingly occurring in sedentary people, and may progress to NASH and hepatocellular carcinoma. It is essential to design affordable animal models for the study of various diseases, including fatty liver, which was the aim of the study. In th...

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Veröffentlicht in:Animal models and experimental medicine 2019-12, Vol.2 (4), p.282-290
Hauptverfasser: Yahaghi, Leyla, Ebrahim‐Habibi, Azadeh, Hayati‐Roodbari, Nasim, Irani, Shiva, Yaghmaei, Parichehreh
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Sprache:eng
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Zusammenfassung:Background Nonalcoholic fatty liver disease (NAFLD) is increasingly occurring in sedentary people, and may progress to NASH and hepatocellular carcinoma. It is essential to design affordable animal models for the study of various diseases, including fatty liver, which was the aim of the study. In this study, a high‐fat diet was devised that triggers NASH's animal model quickly and easily. High‐fat diet (HFD) was used both with intra‐mouth oral gavage and in combination with animal pellets. Methods Twenty‐four male C57BL/6J mice were divided into HFD and ND groups, which received a high‐fat diet and a normal diet, respectively. At the end of the experiment (fourth week of treatment), body and liver weights, biochemical parameters, PPAR‐α gene expression and histopathologic characteristics of the liver were evaluated. Results During 4 weeks, body weight of mice did not show a significant increase in the HFD group compared to the ND group, while weight gain of the liver was significant. Histological assessment of the HFD group's liver confirmed NASH symptoms. In the HFD group, HDL‐c, SOD, catalase, FRAP, adiponectin, and PPAR‐α decreased significantly, and lipid profiles, hepatic enzymes, MDA, leptin, and TNF‐α showed a significant increase compared to the ND group. Conclusion Our high‐fat diet has successfully induced all aspects of NASH with fibrosis in 4 weeks, and with low cost.
ISSN:2576-2095
2096-5451
2576-2095
DOI:10.1002/ame2.12089