Animal models of NASH: getting both pathology and metabolic context right
Date
2008-08-21
Authors
Larter, Claire Z.
Yeh, Matthew M.
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Wiley-Blackwell
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of referral to liver clinics, and its progressive form, non-alcoholic steatohepatitis (NASH), can lead to cirrhosis and end-stage liver disease. The main risk factors for NAFLD/NASH are the metabolic abnormalities commonly observed in metabolic syndrome: insulin resistance, visceral obesity, dyslipidemia and altered adipokine profile. At present, the causes of progression from NAFLD to NASH remain poorly defined, and research in this area has been limited
by the availability of suitable animal models of this disease. In the past, the main models used to investigate the pathogenesis of steatohepatitis have either failed to reproduce the full spectrum of liver pathology that characterizes human NASH, or the liver pathology has developed in a metabolic context that is not representative of the human condition. In the last few years, a number of models have been described in which the full spectrum of liver
pathology develops in an appropriate metabolic context. In general, the underlying cause of metabolic defects in these models is chronic caloric overconsumption, also known as
overnutrition. Overnutrition has been achieved in a number of different ways, including
forced feeding, administration of high-fat diets, the use of genetically hyperphagic animals, or a combination of these approaches. The purpose of the present review is to critique the liver pathology and metabolic abnormalities present in currently available animal models of
NASH, with particular focus on models described in approximately the last 5 years.
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Keywords
hepatic steatosis, high-fat diet, metabolic syndrome, non-alcoholic fatty liver disease, overnutrition
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Journal of Gastroenterology and Hepatology 23.11 (2008): 1635-1648
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Journal article
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