Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease which is characterized by hepatic steatosis and accumulation of lipid in the absence of excess alcohol intake. The current researches are focused on understanding the underlying pathobiology of hepatic steatosis which would promote the development of mechanism-based therapeutic interventions. The occurrence and development of NAFLD is closely associated with the unbalance of uptake of free fatty acid (FFA) from the plasma, de novo lipogenesis, fatty acid oxidation and the secretion of VLDL. Insulin resistance in NAFLD leads to hepatic steatosis by multiple mechanisms. Increased release from an expanded mass of adipose tissue account for greater uptake rates of plasma FFA because of reduced hepatic and adipose tissue insulin sensitivity. Hyperinsulinemia upregulate transcriptional genes that are related with de novo lipogenesis in the liver. The rate of hepatic lipid accumulation exceeds fatty acid oxidation and VLDL secretion. From the four aspects mentioned above, this review will separately discuss the molecular mechanisms by which hepatic triglyceride homeostasis is achieved, as well as the TG metabolic alterations that occur in the setting of insulin resistance and contribute to the pathogenesis of accumulation of TG in NAFLD.