动物造模,小鼠代谢综合征并发脑衰老样病变模型 z-bio 2021-01-14 366

　　Objective: To establish animal models of metabolic syndrome and brain aging-like diseases in C57 mice, and to study their possible mechanisms.

　　Method: 40 C57 mice were randomly divided into 4 groups and 10 normal control groups. There were 10 animals in the low-energy diet group, 10 animals in the high-energy diet group, and 10 animals in the chase group (low-energy diet for 6 weeks, then high-energy diet), and each group of animals was kept for 12 consecutive weeks. At the end of the experiment, the body weight and blood glucose were recorded. Detect biochemical indicators related to metabolic syndrome, calculate insulin resistance index, Westernblot technology to detect the expression levels of age-related protein P53 and phosphorylated P53 (ser15), and observe the deposition of lipoproteins in the hippocampus under an electron microscope Results: The body weight, blood sugar, biochemical indicators related to metabolic syndrome (serum cholesterol, triacylglycerol, insulin-like growth factor 1 and insulin) and the expression levels of P53 and phosphorylated P53 protein were normal in low-energy mice. It was lower than the control group , Lipofuscin has less deposition and high energy. The metabolic syndrome index of the catch-up growth group and the catch-up growth group was significantly higher than that of the control group. The phosphorylation of P53 and P53 protein and the deposition of lipoprotein increased significantly; the insulin resistance of the catch-up growth group was more obvious.

　　 Conclusion: Catching up with diet may induce a mouse metabolic syndrome model with brain senescence-like lesions. This study provides an animal model of metabolic syndrome, as well as a new study to determine the complications caused by changes in their diet.