Non-alcoholic fatty liver disease (NAFLD): The lipid disease of the liver and the effect of statins

Abstract

Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease. Non-alcoholic steatohepatitis (NASH) is the advanced form of NAFLD to which a subpopulation of NAFLD patients progress. While NAFLD is manifested by hepatic steatosis, NASH has the additional features of inflammation, cell injury and ballooning, and mitochondrial changes and/or fibrosis. The understanding of the pathogenesis of NAFLD has been evolving but is still not complete. Fat accumulation in the liver is the first step in the disease process. It occurs when there is increased caloric intake and de novo lipogenesis. Peroxisome proliferator-activated receptors (PPARs), Farnesoid X receptor (FXR) and liver X receptor (LXR) have been shown to play a role in pathogenesis. Many mechanisms are known to be involved in the progress of NAFLD to NASH, including oxidative stress, endotoxins, cytokines, mitochondrial dysfunction and induction of the cytochrome P450 system. More recently discovered possible mechanisms include gut microbiota, dietary fructose, toll-like receptors (TLRs), nucleotide-binding oligomerization domain receptors (NOD-like receptors), and the hedgehog signaling pathway.