Published online Aug 27, 2020. doi: 10.4254/wjh.v12.i8.436
Peer-review started: February 28, 2020
First decision: May 20, 2020
Revised: June 3, 2020
Accepted: June 20, 2020
Article in press: June 20, 2020
Published online: August 27, 2020
Non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disorder in Western countries, comprises steatosis to nonalcoholic steatohepatitis (NASH), with the latter having the potential to progress to cirrhosis. The transition from isolated steatosis to NASH is still poorly understood, but lipidomics approach revealed that the hepatic lipidome is extensively altered in the setting of steatosis and steatohepatitis and these alterations correlate with disease progression. Recent data suggest that both quantity and quality of the accumulated lipids are involved in pathogenesis of NAFLD. Changes in glycerophospholipid, sphingolipid, and fatty acid composition have been described in both liver biopsies and plasma of patients with NAFLD, implicating that specific lipid species are involved in oxidative stress, inflammation, and cell death. In this article, we summarize the findings of main human lipidomics studies in NAFLD and delineate the currently available information on the pathogenetic role of each lipid class in lipotoxicity and disease progression.
Core tip: Lipidomics is a new rapidly growing field that allows the overall and detailed investigation of the whole lipid composition in a given biology matrix. Lipid profiling of liver biopsies of patients with non-alcoholic fatty liver disease (NAFLD) has previously revealed several changes in glycerophospholipids and sphingolipids concentrations and alterations in fatty acid pattern compared to healthy control. However, findings from lipidomics studies in plasma samples are inconsistent. We review the main findings of lipidomics studies and the important pathophysiological role of specific lipid species in lipotoxicity and development of NAFLD.