ArticleExperimental animals2018
A novel hamster nonalcoholic steatohepatitis model induced by a high-fat and high-cholesterol diet.
Article in Experimental animals, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Paradoxical sex differences in a hamster model of angiotensin II-dependent hypertension and associated renal injury.Biology of sex differences · 2025Article
- Diet-induced steatohepatitis does not cause heart failure with preserved ejection fraction in male middle-aged C57BL/6N mice.PloS one · 2025Article
- Downregulation of miR-122-5p Activates Glycolysis via PKM2 in Kupffer Cells of Rat and Mouse Models of Non-Alcoholic Steatohepatitis.International journal of molecular sciences · 2022Article
- Chymase as a Novel Therapeutic Target in Acute Pancreatitis.International journal of molecular sciences · 2021Article
- Article
- Chymase as a Possible Therapeutic Target for Amelioration of Non-Alcoholic Steatohepatitis.International journal of molecular sciences · 2020Review
- The novel mechanism of valproate to prevent peritoneal adhesion formation.Surgery today · 2020Article
- Efficacy and Mechanism of a Chinese Classic Prescription of Yueju in Treating Nonalcoholic Steatohepatitis and Protecting Hepatocytes from Apoptosis.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Comparison of a chymase inhibitor and hyaluronic acid/carboxymethylcellulose (Seprafilm) in a novel peritoneal adhesion model in rats.PloS one · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH), in which there is steatosis and fibrosis in the liver, is linked to metabolic syndrome and progresses to hepatic cirrhosis. In this study, a novel hamster NASH model derived from metabolic syndrome was made using hamsters. Hamsters were fed a normal or a high-fat and high-cholesterol (HFC) diet for 12 weeks. Body weight and the ratio of liver weight to body weight were significantly greater in HFC diet-fed hamsters than in normal diet-fed hamsters. Triglyceride, low-density lipoprotein cholesterol, and glucose levels in blood were significantly increased in HFC diet-fed hamsters, and blood pressure also tended to be high, suggesting that the HFC diet-fed hamsters developed metabolic syndrome. Hepatic steatosis and fibrosis were observed in liver sections of HFC diet-fed hamsters, as in patients with NASH, but they were not seen in normal diet-fed hamsters. Chymase generates angiotensin II and transforming growth factor (TGF)-β, both of which are related to hepatic steatosis and fibrosis, and a significant augmentation of chymase activity was observed in livers from HFC diet-fed hamsters. Both angiotensin II and TGF-β were also significantly increased in livers of HFC diet-fed hamsters. Thus, HFC diet-fed hamsters might develop metabolic syndrome-derived NASH that clinically resembles that in NASH patients.
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