Published online Jul 7, 2020. doi: 10.3748/wjg.v26.i25.3577
Peer-review started: March 18, 2020
First decision: May 15, 2020
Revised: June 18, 2020
Accepted: June 23, 2020
Article in press: June 23, 2020
Published online: July 7, 2020
Dietary oversupply of triglycerides represent the hallmark of obesity and connected complications in the liver such as non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which eventually progress to cirrhosis and hepatocellular carcinoma. Monoacylglycerol lipase is the last enzymatic step in the hydrolysis of triglycerides, generating glycerol and fatty acids (FAs), which are signaling precursors in physiology and disease. Notably, monoacylglycerol lipase (MGL) also hydrolyzes 2-arachidonoylglycerol, which is a potent ligand within the endocannabinoid system, into arachidonic acid - a precursor for prostaglandin synthesis; thus representing a pivotal substrates provider in multiple organs for several intersecting biological pathways ranging from FA metabolism to inflammation, pain and appetite. MGL inhibition has been shown protective in limiting several liver diseases as FAs may drive hepatocyte injury, fibrogenesis and de- activate immune cells, however the complexity of MGL network system still needs further and deeper understanding. The present review will focus on MGL function and FA partitioning in the horizons of liver disease.
Core tip: Monoacylglycerol lipase inhibition/modulation is yet unappreciated however attractive therapeutic concept to limit liver disease as fatty acids may drive hepatocyte injury, fibrogenesis and change immune cells phenotype.