Figure 7.

A self-perpetuating vicious cycle in the development and progression of nonalcoholic fatty liver disease (NAFLD). In the case of hypernutrition, mitochondrial adaptations (e.g., increased mitochondrial fatty acid oxidation, mtFAO) are initiated to curb fat accumulation in livers. However, this adaption secondarily induces excessive reactive oxygen species (ROS) production, thus leading to the aggravation of mitochondrial dysfunction. Underlying mitochondrial dysfunction could further accelerate ROS overproduction and the progression of NAFLD. On the other hand, ROS potentiates the dual role in the initiation of autophagy and suppression of autophagic flux. Overproduction of ROS continuously attacks mitochondria, causing mitochondrial fatigue and mitochondrial decompensation, which promotes lipid overload and lipotoxicity and eventually blocks the autophagic flux. Meanwhile, defective autophagy alters lipid homeostasis, which contributes to the lipid accumulation in liver. In this study, the Chinese herb, Corilagin (Cori) exerts the effects on alleviating lipid deposition in livers of high-fat diet (HFD) induced C57BL/6 mice via diminishing oxidative stress, restoring autophagic flux arrest, as well as improving mitochondrial functions.