Rosiglitazone promotes phosphorylation of AMPK protein and improves insulin resistance in db/db mice
10.19428/j.cnki.sjpm.2020.18883
- VernacularTitle:罗格列酮促进AMPK蛋白磷酸化改善db/db小鼠胰岛素抵抗
- Author:
Na HU
1
;
Lin YUAN
;
Long-juan FANG
;
Yi JIANG
;
Xiao-yu ZHONG
;
Min LIN
;
Min LU
;
Yin-qiang SUN
;
Xiong LU
Author Information
1. Science and Technology Experimental Center of Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
- Publication Type:Research Article
- Keywords:
rosiglitazone;
adenosine 5′-monophosphate-activated protein kinase(AMPK);
glycometabolism;
db/db mice
- From:
Shanghai Journal of Preventive Medicine
2020;32(8):646-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of rosiglitazone on the protein expression of AMPK and GLUT4 in peripheral tissue (liver, skeletal muscle and fat) of type 2 diabetic db/db mice and to prove that rosiglitazone can regulate the glucose metabolism in db/db mice partly through the AMPK pathway. Methods db/db mice were randomly divided into model group and rosiglitazone group according to their blood glucose.The db/m mice were normal control group.After 4 weeks of administration, fasting blood glucose was detected in each group.Western blot was used to detect the contents of AMPK, p-AMPK and GLUT4 in liver, skeletal muscle and adipose tissue. Results (1) Rosiglitazone significantly reduced the fasting blood glucose of db/db mice; (2)Rosiglitazone increased the level of AMPK phosphorylation in the liver, skeletal muscle and adipose tissue of db/db mice, and increased the content of GLUT4 protein in skeletal muscle and adipose tissue. Conclusion Rosiglitazone can increase the phosphorylation of AMPK and the expression of GLUT4 protein in the liver, muscle and fat tissue of db/db mice, and promote the uptake and utilization of glucose in peripheral tissue, suggesting that it can regulate glucose metabolism in db/db mice partly through the AMPK pathway.
