动物造模,代谢综合征并发脑衰老样病变模 z-bio 2021-08-19 534

　　OBJECTIVE: To induce C57 mice to develop metabolic syndrome and brain senescence-like disease animal model by catching up with the growth diet, and to study its possible mechanism.

　　Methods: 40 C57 mice were randomly divided into 4 groups, 10 normal control group, 10 low-energy diet group, 10 high-energy diet group, and catch-up growth group (fed with low-energy diet for 6 weeks before opening high-energy diet) 10 Animals in each group were fed continuously for 12 weeks, body weight and blood glucose were recorded, the metabolic syndrome-related biochemical indicators were detected at the end of the experiment, the insulin resistance index was calculated, Westernblot technology was used to detect the expression levels of aging-related protein P53 and phosphorylated P53 (ser15), electron microscopy Observe the deposition of lipofuscin in the hippocampus.

　　Results: The body weight, blood sugar, metabolic syndrome related biochemical indicators (serum cholesterol, triacylglycerol, insulin-like growth factor 1 and insulin) and the expression levels of P53 and phosphorylated P53 protein in the low-energy group were lower than those in the normal control group. Pigmentation is less; the high-energy group and the catch-up growth group have significantly higher metabolic syndrome indicators than the control group, and there is a significant increase in the expression of P53 and phosphorylated P53 protein and lipofuscin deposition; the catch-up growth group shows more obvious Insulin resistance tendency and brain senescence.

　　Conclusion: Catching-up diet feeding can induce the mouse metabolic syndrome model to complicate brain senescence-like lesions. This study provides new research ideas for the establishment of the metabolic syndrome and its complications neurodegeneration-like changes model caused by dietary changes.