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Non-alcoholic fatty liver disease (NAFLD), the hepatic counterpart of metabolic syndrome, has gained increasing recognition worldwide as a component of the obesity and type 2 diabetes pandemic. The spectrum of NAFLD ranges from simple fatty liver with benign prognosis, to non-alcoholic steatohepatitis (NASH), which may progress to liver fibrosis and cirrhosis, thereby increasing morbidity and mortality. According to the traditional view, hepatic fat accumulation represents the prerequisite for hepatocyte injury to develop, whereas cytokines, adipokines, bacterial endotoxin, mitochondrial dysfunction and/or endoplasmic reticulum stress are described as aggravating factors involved in NASH progression. It is believed that approximately 1%–5% of the Western population exhibit NASH. However, no therapeutic approaches are currently effective in slowing or reversing NASH, and the most promising treatments remain weight loss and exercise. Generating rodent models for preclinical investigations on NASH has been quite challenging over the past years for several laboratories.1–3 The current study of Verbeek et al,4 elegantly validates the long-term use of a high-fat high-sucrose diet (HF-HSD: 40% of saturated fat and 45% of sucrose), also known as Western diet, as a relevant NASH mouse model. Indeed, 12 weeks of HF-HSD diet feeding triggers obesity and insulin resistance in mice, and also leads to liver steatosis accompanied with all clinical features of NASH, namely inflammation, fibrosis, oxidative stress and mitochondrial dysfunction (figure …
Contributors FB wrote the commentary and designed the figure (Servier Medical Art). SG and CP provided scientific inputs and critical comments.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.