Fatty liver when the hepatocytes in the neutral fat ——triglyceride accumulation increased mechanism is complex, summarized in the following reasons. 1, excessive supply of fat in food Long-term and large consumption of high-fat, high-cholesterol diet leads to a large increase in exogenous fat, resulting in the absorption from the small intestine into the blood celiac particles increased, the liver from the blood or synthesis of triglycerides increased successively, although the synthesis of very low-density lipoprotein in hepatocytes also increased accordingly, but still not enough to transfer too much triglycerides into the blood, resulting in triglycerides in the liver cells This leads to abnormal deposition of triglycerides in hepatocytes and the formation of fatty liver. 2. Excessive plasma free fatty acids Growth hormones and glucocorticoids can activate lipase in peripheral adipose tissue, resulting in the hydrolysis of stored fat into glycerol and free fatty acids, and a large number of free fatty acids enter the blood. Compared with those with normal weight, the release of fatty acids into the blood of obese and type 2 diabetic patients is significantly increased, plasma free fatty acids are significantly higher, the uptake of free fatty acids by liver cells from the blood is increased, and the fatty acids used for the synthesis of triglycerides are successively increased. 3.Decrease in cellular fatty acid oxidation utilization If fatty acids can be fully oxidized and converted into energy in hepatocytes, the amount of triglycerides synthesized by hepatocytes will be reduced. When the hepatocyte oxidation of fatty acids is impaired, the hepatocyte will certainly metabolize fatty acids by accelerating the synthesis of triglycerides. Heavy alcohol consumption and the use of certain drugs (such as amiodarone) can inhibit the oxidation capacity of fatty acids in the mitochondria of hepatocytes, making triglyceride synthesis increase, thus making it easy to form a fatty liver. 4, very low density lipoprotein synthesis and excretion disorders in the liver The triglycerides synthesized by hepatocytes are mainly combined with apolipoproteins to form very low density lipoproteins and transferred into the blood. Long-term starvation, poor digestion and absorption, low-protein diet and other reasons for insufficient protein intake, reduced supply of amino acids or lack of essential fatty acids, resulting in insufficient raw materials for synthesis of phospholipids and lipoproteins, which in turn affects the synthesis of lipoproteins; inflammation and necrosis of hepatocytes can cause impaired binding of triglycerides and lipoproteins; tetracycline and certain anti-tumor drugs can reduce the synthesis of apolipoproteins; congenital impaired synthesis of apolipoproteins and long-term colchicine administration can cause impairment of hepatocyte microtubule structure and function. All of the above causes can lead to the inability of triglycerides synthesized in hepatocytes to be successfully transported into the blood, and fat accumulation in hepatocytes can occur despite the fact that triglyceride synthesis is not increased. In conclusion, any cause of imbalance between triglyceride synthesis and very low density lipoprotein secretion in hepatocytes can lead to abnormal fat deposition in hepatocytes, resulting in fatty liver.