Larter, Claire Z.Yeh, Matthew M.2012-04-042012-04-040815-93191440-1746http://hdl.handle.net/1885/8966Non-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.This research was funded through a grant. - Research in the authors' laboratory is supported by program grant 358398 from the Australian National Health and Medical Research Council (NHMRC).15 pageshttp://www.sherpa.ac.uk/romeo/issn/0815-9319/ From February 2007 "Author can archive pre-print … [and] post-print subject to restrictions: If signed CTA, only allowed with written permission [and] 0-24 months [embargo] depending on journal … Cannot archive publisher's version/PDF. [and] Please see former John Wiley & Sons and Blackwell Publishing policies for articles published prior to February 2007; Publisher source must be acknowledged with citation; Must link to publisher version with set statement [The definitive version is available at www3.interscience.wiley.com]" - from SHERPA/RoMEO site (as at 04/04/12)hepatic steatosishigh-fat dietmetabolic syndromenon-alcoholic fatty liver diseaseovernutrition2008-08-2110.1111/j.1440-1746.2008.05543.x2015-12-08