Published online Sep 10, 2019. doi: 10.4291/wjgp.v10.i2.11
Peer-review started: May 20, 2019
First decision: August 2, 2019
Revised: August 9, 2019
Accepted: August 21, 2019
Article in press: August 21, 2019
Published online: September 10, 2019
Processing time: 114 Days and 14.9 Hours
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. NAFLD is known to be associated with obesity, type 2 diabetes, metabolic syndrome and increased cardiovascular events: for these reasons, it is becoming a global public health problem and represents an important challenge in terms of prevention and treatment. The mechanisms behind the pathogenesis of NAFLD are multiple and have not yet been completely unraveled; consequently, at moment there are not effective treatments. In the past few years a large body of evidence has been assembled that attributes an important role in hepatic aberrant fat accumulation, inflammation and fibrosis, to the vitamin D/vitamin D receptor (VD/VDR) axis, showing a strong association between hypovitaminosis D and the diagnosis of NAFLD. However, the data currently available, including clinical trials with VD supplementation, still provides a contrasting picture. The purpose of this editorial is to provide an overview of recent advances in the pathogenesis of NAFLD in relation to VD/VDR. Based on recent data from literature, we focused in particular on the hypothesis that VDR itself, independently from its traditional ligand VD, may have a crucial function in promoting hepatic fat accumulation. This might also offer new possibilities for future innovative therapeutic approaches in the management of NAFLD.
Core tip: In the last years, many evidences attribute to the vitamin D/vitamin D Receptor axis an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The purpose of this editorial is to provide an overview of recent advances in the pathogenesis of NAFLD in relation to vitamin D/vitamin D receptor (VD/VDR). We focused in particular on the hypothesis that VDR itself, independently from its traditional ligand VD, may play a crucial function in promoting hepatic fat accumulation, also offering new possibilities for innovative therapeutic approaches in the management of NAFLD.