Non-alcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide and comprises varied grades of intrahepatic lipid accumulation, inflammation, ballooning, and fibrosis; the most severe cases result in cirrhosis and liver failure. There is extensive clinical and experimental evidence indicating that chronic intermittent hypoxia, featuring a respiratory disorder of growing prevalence worldwide termed obstructive sleep apnea, could contribute to the progression of NAFLD from simple steatosis, also termed non-alcoholic fatty liver or hepatosteatosis, to non-alcoholic steatohepatitis; however, the molecular mechanisms by which hypoxia might contribute to hepatosteatosis setup and progression still remain to be fully elucidated. In this review, we have prepared an overview about the link between hypoxia and lipid accumulation within the liver, focusing on the impact of hypoxia on the molecular mechanisms underlying hepatosteatosis onset.

Hepatitis C virus (HCV) is still considered as a major public health problem because in 2015 around 71 million people were chronically infected worldwide. It is important to note that chronic HCV infection is a systemic disease that is associated with diverse extrahepatic disorders including insulin resistance and type 2 diabetes mellitus. The discovery of new direct-acting antiviral agents (DAAs) has become a huge advance in the treatment of HCV infection. The complex interplay between HCV and glucose metabolic pathways remains to be fully elucidated, but it is becoming clearer that elimination of chronic HCV infection halts the progression of liver disease, but more evidence is still needed to better understand how successful antiviral treatment influences insulin resistance and other abnormalities of glucose metabolism linked to HCV infection. This review provides a comprehensive overview of the glucose metabolism disturbances related to chronic HCV infection, highlighting the new insights into the molecular basis of insulin resistance induced by HCV and the mechanisms underlying the reversion of this metabolic disorder by DAAs.