Figure 1.

Hypothetic mechanism of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) progression. Excessive intake of excess calories and fat results in accumulation of triglycerides, total cholesterol, and free fatty acids, inducing hepatic steatosis. The overload of liver lipids enhances lipid peroxidation, which induces the production of reactive oxygen species and steatohepatitis. Hepatic inflammation activates the mitogen-activated protein kinase pathway and nuclear factor-κB, resulting in insulin resistance. Insulin resistance also promotes de novo lipogenesis, forcing the healthy liver to develop NASH. The inflammation also recruits Kupffer cells and polarizes M1 macrophages, activating hepatic stellate cells and finally leading to liver fibrosis. TG, triglycerides; TC, total cholesterol; FFA, free fatty acids; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB.