动物造模 z-bio 2022-10-31 308

　　Objective To evaluate the role of GIP receptor (GIPR) signal transduction in insulin resistance and liver steatosis in mouse model adipose tissue by ultrasound.

　　Methods Sixteen 4-week old GIPR knockout (GIPRadipo -/-) and wild-type (WT) mice were selected and fed with normal fat diet (CFD) and high fat diet (HFD) for 15 weeks. The weight changes of mice were recorded. After feeding for 5, 8, 10, 12 and 15 weeks, the blood glucose, insulin and total GIP levels of mice were recorded; Real time quantitative RT-PCR was used to determine the changes of inflammatory cytokines in mouse adipose tissue and the expression of related genes in GIPR signal transduction pathway; The volume, weight and fat content of liver in mice were quantitatively evaluated by ultrasound; Western blot analysis was used to evaluate Akt phosphorylation in fat, liver and skeletal muscle tissues after insulin treatment.

　　Results Compared with WT mice, the weight of GIPRadipo -/- mice fed with HFD significantly decreased. HFD fed GIPRadipo -/- mice reduced insulin resistance, liver weight, and liver steatosis. Compared with WT mice fed with HFD, GIPRadipo -/- mice had lower levels of plasma interleukin-6 (IL-6).

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