动物造模,巨噬细胞 Z-bio 2022-12-26 337

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

　　Methods Eight week old SPF grade male macrophages MED1 knockout (MED1 Δ Mac) and wild type (MED1fl/fl) mice were fed with high-fat diet for 0, 4, 8, 12, 16 and 20 weeks to induce obesity and insulin resistance. Body weight, total triglyceride (TG), total cholesterol (TC) and blood glucose levels were dynamically measured at 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 Compared with MED1fl/fl control group, MED1 Δ The weight of Mac mice tended to increase, but there was no significant difference, and there was no difference in plasma TC and TG between the two groups. There was no significant difference in blood glucose between the two groups at 0, 4, 8, 12 and 16 weeks of high-fat diet, but at 20 weeks, MED1 Δ The blood sugar of Mac mice increased significantly (P<0 01), liver steatosis is enhanced, and MED1 Δ The liver weight, subcutaneous fat and visceral fat of Mac mice all increased. Further glucose tolerance test (GTT) and insulin tolerance test (ITT) showed that there was no significant difference between the two groups in grape tolerance and insulin sensitivity.

　　Conclusion Macrophage MED1 deletion can increase blood glucose level and liver steatosis, but has no significant effect on insulin resistance, suggesting that macrophage MED1 may play a key role in regulating glucose metabolism.