**5. Conclusion**

The mechanisms associated with the deposition and maintenance of excess hepatic lipids define an imbalance between the hepatic production and removal of TGs, which are majorly transferred from the liver within VLDLs. Data concerning which toxic lipids induce liver injury in NAFLD and NASH are limited. Agents or factors that stimulate or modulate liver damage in NAFLD can assist to identify potential therapeutic targets. HDLs have been recognized as good cholesterol, essential to the body, which functions to ameliorate various metabolic conditions, including CVDs and NAFLD. Correction and management of the factors involved in the pathophysiology and progression of NAFLD, including hyperlipidaemia, obesity, IR, DM, oxidative stress, lifestyle, inactivity and poor dietary control are the current therapeutic targets for NAFLD. To minimize liver damage in NAFLD, new approaches that target HDL-induced drugs and cholesterol metabolism pathways may be helpful in lowering hepatic cholesterol content.
