Fatty liver, a group of metabolic diseases with excessive fat deposition in the liver, is precisely a clinicopathological syndrome characterized by fatty degeneration of hepatocytes. Fatty liver can be an independent primary disease, but it is more often a manifestation of some systemic diseases involving the liver, especially considered an important manifestation of the metabolic syndrome, and therefore often co-exists with diabetes, obesity, and hypertensive disorders, exacerbating each other. In fact, lipids are also present in hepatocytes, and in fatty liver, these lipids accumulate more than 5% of the wet weight of the liver, or pathologically more than 1/3 of the hepatocytes per unit area have lipid droplets present, and in severe cases the liver lipid content is even up to 40%-50% of the wet weight of the liver, with or without clinical signs associated with liver disease. These lipids include triglycerides, phospholipids, glycolipids or cholesterol lipids, but the vast majority is due to the accumulation of triglycerides. So, how does a fatty liver develop? That is, how do lipids get deposited in excess in the liver cells? This starts from the absorption and metabolism of lipids. If a large amount of high-fat and high-cholesterol food is eaten, the celiac particles that enter the blood after absorption from the small intestine increase, and the liver takes in or synthesizes triglycerides from the blood successively, which is one source of triglycerides, and another source is the fatty tissue outside the liver. In obese and type 2 diabetic patients, the excessive peripheral fatty tissue in the body is broken down by lipase into fatty acids In obese and type 2 diabetic patients, the excess peripheral adipose tissue is significantly increased by the breakdown of fatty acids by lipase, and the uptake of free fatty acids from the blood by hepatocytes is increased, and the fatty acids used for triglyceride synthesis are successively increased. Alcohol consumption disrupts the oxidative utilization of fatty acids and is more converted to triglycerides deposited in the liver. The triglycerides synthesized by hepatocytes are mainly bound to apolipoproteins to be transported into the blood in the form of very low density lipoproteins. For various reasons, such as malnutrition, drugs, hepatitis and other factors can lead to impaired synthesis of very low density lipoproteins, then triglycerides lack transport means, can not be transported to the liver in time to use, then too much deposition in the liver cells, the formation of fatty liver, so it can be seen that any cause of the imbalance between the synthesis of triglycerides and the secretion of very low density lipoproteins in the liver cells, can lead to abnormal fat in the liver cells Therefore, it can be seen that any imbalance between triglyceride synthesis and low-density lipoprotein secretion in hepatocytes can lead to abnormal deposition of fat in hepatocytes, resulting in fatty liver. Clinically, fatty liver has an insidious onset and often presents with asymptomatic liver enlargement and persistent mild elevation of serum transaminases. Some alcoholic and diabetic fatty livers may sometimes present with discomfort or pain in the right upper abdomen due to intracellular fat deposits. A small proportion has an acute onset, often with extensive metabolic dysfunction and a clinical presentation similar to that of acute or subacute severe viral hepatitis. The diagnosis is based on laboratory tests, including laboratory tests, ultrasound and CT, and liver aspiration if necessary. Laboratory tests include normal or mildly abnormal liver function glutamic or glutamic aminotransferase, transpeptidase may be elevated, especially in alcoholic fatty liver; blood lipids are often elevated; ultrasound examination is seen in large liver with reduced echogenicity, fatty liver with intrahepatic fat content of 30% or more can be detected by ultrasound, and fatty liver with liver fat content of 50% or more can be diagnosed with ultrasound sensitivity of more than 90%, ultrasound as a non-invasive test can be repeatedly examined The ultrasound is a non-invasive test that can be repeatedly checked, especially during the treatment process to determine the efficacy of the treatment. Although liver tissue examination is not yet comparable in determining inflammation, steatosis and fibrosis in the liver, liver biopsy is generally not advocated as a routine measure to confirm the diagnosis of nonalcoholic steatohepatitis at home and abroad due to the benign course of most patients with nonalcoholic steatohepatitis, the lack of effective prevention and treatment measures and the risks involved after diagnosis. Treatment consists of three aspects, like a “triad” – diet, exercise and medication. Diet therapy is mainly to control the total calories, pay attention to the diet structure, eat more coarse grains, vegetables, less greasy, fried and animal food; exercise therapy can effectively reduce visceral fat, improve insulin resistance, and thus reduce fat deposition in the liver, for patients with fatty liver with elevated transaminases, less activity and more rest is not a wise approach, the only way to promote the recovery of liver function as soon as possible is to strengthen exercise. For patients with simple fatty liver, steatohepatitis and hyperlipidemia that cannot be improved by diet and exercise therapy, they need to be treated with medication, including lipid-lowering drugs and liver-protective drugs, and fatty liver with combined diabetes and hyperlipidemia can be treated with polyphosphocholine, silymarin, vitamin E and chitosan capsules. Or until the biochemical index of liver function is normalized and/or the imaging examination shows that the fatty liver has subsided, Chinese medicine also has a wide range of applications and development prospects.