Multiple organs involved in the pathogenesis of non-alcoholic fatty liver disease

摘要

Inter-organ crosstalk regarding the pathogenesis mechanism of NAFLD. The adipose tissue contributes fatty acids to facilitate hepatic steatosis and also produces cytokines to impact proinflammatory pathways, which in turn exacerbates obesity, insulin resistance, adipocyte death and lipolysis. Adipokines deliver metabolic signals to the brain as well. Gut dysbiosis affects gut hormones, metabolites and bacterial components, which subsequently influence the development and progression of NAFLD. Moreover, gut hormones could also interact with different neurons of the brain, to influence appetite and energy homeostasis. The central nerve system integrates hormonal and neurol signals from peripheral organs to control energy balance, which when impaired leads to obesity and NAFLD. It also remarkedly influences lipogenesis and lipolysis by mastering biological clocks and modulating adipose activities. Consequently, in the liver, lipodystrophy may result in ROS production, mitochondrial dysfunction, ER stress, apoptosis, inflammation, hepatokine dysregulation, and autophagy, thus collectively inducing the development of NAFLD