动物造模,巨噬细胞 z-bio 2022-06-16 508

　　Objective To study the regulatory role of macrophage MED1 in the occurrence of insulin resistance.

　　Methods 8-week-old SPF-grade male macrophage MED1 knockout (MED1ΔMac) and wild-type (MED1fl/fl) mice were used as models, and were fed a high-fat diet for 0, 4, 8, 12, 16 and 20 weeks to induce Obesity and insulin resistance occur. Body weight, total triglyceride (TG), total cholesterol (TC) and blood glucose levels were dynamically detected during different periods of high-fat diet feeding. After 20 weeks of high-fat feeding, the pathological changes of liver and adipose tissue were observed by hematoxylin-eosin (HE) staining.

　　Results After high-fat diet feeding, compared with MED1fl/fl control mice, the body weight of MED1ΔMac mice increased, but there was no significant difference, and there was no difference in plasma TC and TG between the two groups of mice. There was no significant difference in blood glucose between the two groups at 0, 4, 8, 12, and 16 weeks of high-fat diet feeding, but at 20 weeks, blood glucose in MED1ΔMac mice was significantly increased (P < 0.01), and liver fat was significantly higher in MED1ΔMac mice. Degeneration was enhanced, and liver weight, subcutaneous fat, and visceral fat all tended to increase in MED1ΔMac mice. Further glucose tolerance test (GTT) and insulin tolerance test (ITT) showed that there was no significant difference in grape tolerance and insulin sensitivity between the two groups of mice.

　　Conclusion The deletion of MED1 in macrophages promotes increased blood glucose levels and hepatic steatosis, but has no significant effect on insulin resistance, suggesting that MED1 in macrophages may have a key regulatory role in glucose metabolism.