Fig. 2. The pathophysiology of NASH.

There are four main molecular mechanisms of NASH: (i) Under insulin resistance, fructose could be converted to triglycerides thereby facilitating DNL. Insulin resistance in adipose tissue can cause adipokine distribution disorder and induce liver inflammation; (ii) Mitochondrial dysfunction leads to excessive production of ROS and TNF-α to trigger JNK, which induces the release of pro-apoptotic Smac/Diablo protein; (iii) Two characteristics of NASH are the production of foamy KCs and cholesterol crystals in liver cells; (iv) Bacteroides are independently related to NASH while Ruminococcus is independently related to clinically obvious fibrosis.