Experimental models of non-alcoholic fatty liver disease in rats

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the Western world, and it persists at a high prevalence. NAFLD is characterised by the accumulation of triglycerides in the liver and includes a spectrum of histopathological findings, ranging from simple fatty liver through non-alcoholic steatohepatitis (NASH) to fibrosis and ultimately cirrhosis, which may progress to hepatocellular carcinoma. The pathogenesis of NAFLD is closely related to the metabolic syndrome and insulin resistance. Understanding the pathophysiology and treatment of NAFLD in humans has currently been limited by the lack of satisfactory animal models. The ideal animal model for NAFLD should reflect all aspects of the intricate etiopathogenesis of human NAFLD and the typical histological findings of its different stages. Within the past several years, great emphasis has been placed on the development of an appropriate model for human NASH. This paper reviews the widely used experimental models of NAFLD in rats. We discuss nutritional, genetic and combined models of NAFLD and their pros and cons. The choice of a suitable animal model for this disease while respecting its limitations may help to improve the understanding of its complex pathogenesis and to discover appropriate therapeutic strategies. Considering the legislative, ethical, economical and health factors of NAFLD, animal models are essential tools for the research of this disease.

Effects of a combination of puerarin, baicalin and berberine on the expression of proliferator-activated receptor-γ and insulin receptor in a rat model of nonalcoholic fatty liver disease

“…The high-fat diet model has been widely used in previous NAFLD studies (39,40). The histological results of the present study observed NAFLD features in the model rats, indicating that an NAFLD model was successfully generated.…”

Metformin improves hepatic IRS2/PI3K/Akt signaling in insulin-resistant rats of NASH and cirrhosis

“…Dietary-induced NAFLD rodent models, which vary in diet compositions, duration of feeding, animal strain, sex, and age, are the most widely used according to the previous studies (Kucera & Cervinkova 2014). A variety of genetic models of NAFLD are more expensive and less available (Qi et al 2005, Nagarajan et al 2012.…”

Protective effect of ursodeoxycholic acid, resveratrol, andN-acetylcysteine on nonalcoholic fatty liver disease in rats

“…This animal model of steatosis was based mainly on the model reported by Delzenne et al (1997) with diet fed being MCDD instead of a high-fructose fat-free diet (Kucera & Cervinkova, 2014) because on using fructose alone liver inflammation does not occur in a pattern consistent with human fatty liver (Lee et al, 2007). UDCA, RSV, and NAC were dissolved in water and given daily by the oral route through an orogastric catheter at doses of 25, 10, and 20 mg/kg/d, respectively (Bujanda et al, 2008;Mas et al, 2008;Samuhasaneeto et al, 2007).…”