Abstract
Nonalcoholic fatty liver disease (NAFLD) is now the leading cause of chronic liver disease in western countries. The molecular mechanisms leading to NAFLD are only partially understood, and effective therapeutic interventions are clearly needed. Therefore, preclinical research is required to improve knowledge about NAFLD physiopathology and to identify new therapeutic targets. Primary human hepatocytes, human hepatic cell lines, and human stem cell-derived hepatocyte-like cells exhibit different hepatic phenotypes and have been widely used for studying NAFLD pathogenesis. In this paper, apart from employing the different in vitro cell models for the in vitro assessment of NAFLD, we also reviewed other approaches (metabolomics, transcriptomics, and high-content screening). We aimed to summarize the characteristics of different cell types and methods and to discuss their major advantages and disadvantages for NAFLD modeling.
Highlights
IntroductionNonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in western countries, affecting 17–46% of adults and characterized by increased fat accumulation [1]
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in western countries, affecting 17–46% of adults and characterized by increased fat accumulation [1].NAFLD comprises two different histological forms: nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) [2]
104 differentially expressed proteins as indicators of enhanced protein synthesis accompanied by a down-regulation of histones
Summary
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in western countries, affecting 17–46% of adults and characterized by increased fat accumulation [1]. NAFLD comprises two different histological forms: nonalcoholic fatty liver (or simple steatosis) and nonalcoholic steatohepatitis (NASH) [2]. Steatosis can be defined as the presence of increased fat accumulation in the liver without hepatocellular necrosis and no, or minimal, inflammation. NASH is characterized by steatosis, liver inflammation, and hepatocyte ballooning with or without fibrosis. The progression of NASH underlies cirrhosis and hepatocellular carcinoma [2]. Evidence for hepatic steatosis in the absence of other causes of liver fat accumulation (i.e., significant alcohol consumption or hereditary disorders) is required to diagnose
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