Nonneurological aspects of the endocannabinoid system: Nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a global leading cause of the increased incidence of liver mortality and morbidity. It has been reported that the implication of the endocannabinoid system in the pathogenesis of NAFLD may be due to the activation of the cannabinoid receptors CB1 and CB2 via the increased fat influx to the liver. This inhibits fatty acid oxidation and leads to the activation of some transcriptional factors, including sterol regulatory element binding protein (SREBP-1c) and stearoyl-CoA desaturase (SCD1), involved in lipogenesis. The overexpression of CB1 may be due to lipid metabolism dysregulation, while a high CB2 expression is possibly due to the increases levels of some proinflammatory cytokines during nonalcoholic steatohepatitis (NASH). Cannabis use in treating some diseases, including NAFLD, is attracting considerable interest due to the positive impact on CB1 receptors. This chapter sheds light on the implication of the endocannabinoid system in the pathogenesis of NAFLD and whether the use of cannabis is effective in treating NAFLD.