动物造模,药效评价,糖尿病 z-bio 2024-08-06 803

　　Diabetes mice: It was first reported by Hummel et al. (1966) that it was caused by a recessive mutation gene and spontaneously originated from inbred mice (C57BL/Ks) in Jackson's laboratory. This gene (db) and obesity (ob) are not alleles, but located on chromosome 4 (gene cluster 8).

　　[Result analysis] Homozygous diabetes mice (db/db) showed signs at 3-4 weeks of age. The first expression of db/db gene mice was that when the diseased mice reached 3-4 weeks of age, there was abnormal fat deposition in the subcutaneous tissues of axilla and groin, at which time the blood sugar increased. This type of mouse has a tendency towards excessive obesity. When the diabetes mice are 3 to 8 weeks old, their weight increases rapidly, sometimes reaching about 45g (the normal mice weigh about 12 to 20g). Then the weight of the mice began to gradually decrease until they developed symptoms and died.

　　Obesity is often associated with overeating and can also lead to hyperglycemia in clinical practice. At 4 weeks of age, the blood glucose concentration of this type of mouse reaches 300mg/100ml of blood, and at 12 weeks of age, the blood glucose level can reach as high as 500mg/100ml of blood. When the blood glucose level in mice exceeds 250mg/100ml of blood, some clinical symptoms appear, such as diabetes, polyuria, and polydipsia. The blood glucose level of normal mice is generally 140-180mg/100ml blood.

　　The content of insulin in blood of young diabetes rats was different. During childhood, insulin levels in the plasma of mice gradually increase until around 8 weeks of age, and then gradually decrease to normal levels. After 12 weeks of age, the content of mice only remained at about 25% of the normal amount until they became diseased and died. The life span of diabetes mice is relatively short, about 4-6 months. Most mice cannot survive for more than 8 months, but early dietary control can prolong their lifespan. The clinical symptoms of diabetes mice (db/db) include obesity, hyperglycemia, diabetes, proteinuria, thirst, polyuria, and finally death due to ketonuria. Pathological changes of kidney, lung, heart and eyes are rare. Only pancreatic islets have obvious diabetes changes, and B-cells of pancreatic islets show degeneration and particle reduction. Like et al. (1972) described the changes in the glomeruli of db/db mice, which were similar in appearance to normal mice of the same age, but much larger than the latter. When the mice reached the age of onset of diabetes, the changes in the glomeruli were more obvious. This diabetes mouse (C57BL/KsJ db/db) is an ideal animal model for studying human diabetes at present.