Figure 1. An overview of the pathophysiological mechanisms underlying NASH.

Hepatic steatosis results from imbalance between lipid supply (dietary lipids, adipose lipolysis and de novo lipogenesis) and utilization (fatty acid β oxidation and VLDL secretion) by hepatocytes. Insulin resistance, adipose tissue dysfunction, and excess dietary fructose drive hepatic steatosis, which predisposes hepatocytes to injury and cell death in the presence of other stress signals and pathogenic insults. Liver injury triggers remodeling of the immune and stromal vascular microenvironment that results in chronic tissue inflammation and liver fibrosis.