动物模型,动物造模,脂肪肝 z-bo 2022-02-02 484

　　[Modeling mechanism] Mutations in genes key to fat metabolism in liver cells can cause abnormal fat metabolism and disrupt the balance of fat input/output in the liver.

　　[Characteristics of the model] Ob/ob mouse (ob/obmice) is a recessive genetic mutant mouse discovered in the Jackson Laboratory in the United States in 1949. Currently, it is the most commonly used NAFLD model abroad. Due to spontaneous mutations in the ob gene, ob/ob mice cannot synthesize leptin. The ob gene encodes the hormone leptin that suppresses appetite, leading to overeating, obesity, hyperinsulinemia, hyperlipidemia, and obvious hyperglycemia. Histopathological changes include fatty degeneration of liver cells, etc. (Figure 7-2 / Color at the end of Figure 7-2). Normal feed intake only occurs in simple fatty liver, unless methionine and choline deficiency or high-fat diet or coexist with other liver disease factors, otherwise it will not develop into non -alcoholic hepatitis (NASH). db/db mice or fa/fa (Zucker) rats are caused by mutations in the db gene (or fa gene) of the leptin receptor, which causes leptin resistance, and is similar to ob/ob mice . Phenotype.

　　FLS mouse (fatty livershionogimouse) is a new fatty liver strain, without the overeating, obesity and diabetes reported by Soga and Equivalent through inbreeding in 1999. Small fat particles accumulate in the liver lobules of newborn FLS mice and gradually increase with age. The liver triglyceride (TG) content is five times that of ddShionogi (DS) mice of the same age, but blood lipids are no exception. After 2 to 4 months, the foam cells had accumulated monocytes that infiltrated the liver of FLS mice, and serum aminotransferase levels increased. At 4 to 6 months of age, the number of large lipid droplets in the liver cells of FLS mice decreases, and 12-month-old FLS mice develop spontaneous hepatocellular adenoma (HCA) or hepatocellular carcinoma (HCC). Tend to .