动物造模 z-bio 2023-03-13 446

　　Objective To investigate the role of GIP receptor (GIPR) signaling in adipose tissue in a mouse model of insulin resistance and hepatic steatosis assessed by ultrasound.

　　Methods 16 4-week-old GIPR gene knockout (GIPRadipo-/-) and wild-type (WT) mice were selected and fed with normal fat diet (CFD) and high fat diet (HFD), 8 mice in each group, and fed 15 mice continuously. week. The weight changes of mice were recorded. After 5, 8, 10, 12 and 15 weeks of feeding, the blood glucose, insulin and total GIP levels of mice were recorded; real-time quantitative RT-PCR was used to measure the related inflammatory cytokines and GIPR in mouse adipose tissue. Changes in expression of related genes in signaling pathways; quantitative assessment of mouse liver volume, liver weight, and liver fat content by ultrasound; Akt phosphorylation in adipose, liver, and skeletal muscle tissue after insulin treatment by western blot analysis .

　　Results Under HFD-fed conditions, the body weight of GIPRadpo-/- mice was significantly reduced compared with WT mice. HFD-fed GIPRadipo-/- mice had reduced insulin resistance, liver weight, and hepatic steatosis. Plasma interleukin 6 (IL-6) was decreased in GIPRadpo-/- mice compared with HFD-fed WT mice.

　　Conclusion GIPR signaling in adipose tissue plays a key role in HFD-induced insulin resistance and hepatic steatosis in vivo, which may involve IL-6 signaling.