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Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disease in the Western countries affecting 20%–30% of the general population. NAFLD is considered as one of the manifestations of the metabolic syndrome, closely associated with obesity and type 2 diabetes, and may range from steatosis to the more aggressive form of non-alcoholic steatohepatitis (NASH). Long-standing NASH may progress in severe form of liver diseases, such as cirrhosis and hepatocellular carcinoma.
Steatosis in the liver is characterised by a large intracytoplasmic or well-defined fat droplets accumulation, displacing the nucleus to the cell periphery. Abnormal hepatic triglyceride accumulation is due to dysregulation of fatty acid metabolism. In healthy conditions, fatty acids are preferably stored in adipose tissue. However, elevated peripheral fatty acids together with hepatic de novo lipogenesis and defective apolipoprotein biosynthesis lead to hepatic lipid accumulation.
In this issue, Guillou and colleagues identify a novel hepatic-specific mechanism in the pathogenesis of NAFLD that directly involves the fatty acid sensor peroxisome proliferation-activated receptor α (PPARα) and the hormone fibroblast growth factor 21 (FGF21).1
PPARs are ligand-activated transcription factors belonging to the nuclear receptor subfamily. They act as lipid sensors, regulating almost every aspect of lipid metabolism. Functional impairment or dysregulation of these receptors leads to obesity, fatty liver and type 2 diabetes. Although the three PPAR isoforms (α, β/δ and γ) share structural similarity and high homology sequence, they are …
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