Figure 2.

Association between obstructive sleep apnea and the development and evolution of non-alcoholic fatty liver disease. Intermittent hypoxia leads to tissue hypoxia, OS, mitochondrial dysfunction, inflammation, and overactivation of the sympathetic nervous system (SNS). Generated reactive O₂ species (ROS) may amplify liver injury by activating hypoxia-inducible factor 1, a transcriptional activator and master regulator of O₂ homeostasis during hypoxia, and by up-regulating nuclear factor κ-light-chain enhancer of activated B cells (NF-κB), with subsequent downstream induction of inflammatory pathways. As a consequence, this involves insulin resistance, dysfunction of key steps in hepatic lipid metabolism, atherosclerosis, and hepatic steatosis and fibrosis, each of which is pertinent to the development and/or progression of non-alcoholic fatty liver disease (NAFLD) (98–101).