Table 1.
Study/Animal Model | Diet | Age | Stage Disease | Mechanism |
---|---|---|---|---|
Cote el al., 2013 [19] Sprague–Dawley rats | 40% fat and 1.25% cholesterol | 8-week-old female | Fatty liver disease | Hepatic accumulation triglycerides and cholesterol Decreased FXRs Lower expression of HMG-CoA-r, FDFT1, and ABCG8 |
Ichimura et al., 2015 [20] Sprague–Dawley rats | Fat alone or in combination with 1.25% or 2.5% cholesterol | 9-week-old male | Hepatic steatosis | Diminished CPT activity and ABCG5 |
Moriya et al., 2012 [21] SHRSP5/Dmcr rats | High-fat diet | 10-week-old male | Hepatic fibrotic and inflammatory status of NASH | Altered TNFα proinflammatory cytokine and NFkB pathways |
Yeti et al., 2013 [22] SHRSP5/Dmcr rats |
Fat and cholesterol High-fat high-cholesterol diet |
Male SHRSP5/Dmcr rats at 10 weeks old | Phenotype similar to NASH in humans Inflammatory fibrotic liver disease Hepatocyte necrosis |
Downregulation of caspase activity |
Horai et al., 2016 [23] SHRSP5/Dmcr rats | High cholesterol | 6-week-old male rats | Hepatic steatosis, inflammation, and fibrosis | Eosinophilic inclusion bodies and mega-mitochondria |
HMG-CoA-r: 3-hydroxy-3-methylglutaryl coenzyme A reductase; FXR: farnesoid X receptor; FDFT1: farnesyldiphosphate farnesyl-transferase 1; ABCG8: adenosine triphosphate-binding cassette transporter G8; NFkB: nuclear factor kappa B; CPT: carnitine palmitoyltransferase.