胡娜, 袁琳, 方龙娟, 姜逸, 钟霄毓, 林敏, 陆敏, 孙银强, 陆雄. 罗格列酮促进AMPK蛋白磷酸化改善db/db小鼠胰岛素抵抗[J]. 上海预防医学, 2020, 32(8): 646-650. DOI: 10.19428/j.cnki.sjpm.2020.18883
引用本文: 胡娜, 袁琳, 方龙娟, 姜逸, 钟霄毓, 林敏, 陆敏, 孙银强, 陆雄. 罗格列酮促进AMPK蛋白磷酸化改善db/db小鼠胰岛素抵抗[J]. 上海预防医学, 2020, 32(8): 646-650. DOI: 10.19428/j.cnki.sjpm.2020.18883
shu
HU Na, YUAN Lin, FANG Long-juan, JIANG Yi, ZHONG Xiao-yu, LIN Min, LU Min, SUN Yin-qiang, LU Xiong. Rosiglitazone promotes phosphorylation of AMPK protein and improves insulin resistance in db/db mice[J]. Shanghai Journal of Preventive Medicine, 2020, 32(8): 646-650. DOI: 10.19428/j.cnki.sjpm.2020.18883
Citation: HU Na, YUAN Lin, FANG Long-juan, JIANG Yi, ZHONG Xiao-yu, LIN Min, LU Min, SUN Yin-qiang, LU Xiong. Rosiglitazone promotes phosphorylation of AMPK protein and improves insulin resistance in db/db mice[J]. Shanghai Journal of Preventive Medicine, 2020, 32(8): 646-650. DOI: 10.19428/j.cnki.sjpm.2020.18883
shu

罗格列酮促进AMPK蛋白磷酸化改善db/db小鼠胰岛素抵抗

Rosiglitazone promotes phosphorylation of AMPK protein and improves insulin resistance in db/db mice

    摘要
  • 摘要:
    目的观察罗格列酮对2型糖尿病db/db小鼠肝脏、骨骼肌和脂肪中5′-单磷酸腺苷活化蛋白激酶(AMPK)和葡萄糖转运蛋白4(GLUT4)的蛋白表达的影响，了解罗格列酮调节AMPK信号通路的初步机制。
    方法将db/db小鼠按血糖浓度随机分层分为模型组和罗格列酮组；同窝出生的db/m小鼠为正常对照组。灌胃给药4周(罗格列酮5 mg/kg，其余组给予同等剂量的生理盐水)，分别于用药2周和4周后检测小鼠的空腹血糖；用药4周末处死动物，立即取肝脏、皮下脂肪组织和腓肠肌，置于-80 ℃环境保存，用免疫印迹试验(Western blot)检测AMPK、p-AMPK以及GLUT4的蛋白表达。
    结果① 罗格列酮显著降低db/db小鼠的空腹血糖浓度。用药2周后模型组血糖浓度为(22.09±3.67)mmol/L，罗格列酮组血糖浓度为(14.18±3.59)mmol/L(P＜0.05)；用药4周后模型组血糖浓度为(23.08±3.66)mmol/L，罗格列酮组血糖浓度为(14.18±3.59) mmol/L(P＜0.01)；②罗格列酮可上调db/db小鼠肝脏、骨骼肌和脂肪组织AMPK磷酸化水平，增加骨骼肌和脂肪组织的GLUT4蛋白含量。
    结论罗格列酮可增加db/db小鼠肝脏、肌肉和脂肪组织AMPK的磷酸化和GLUT4的蛋白表达，促进外周组织的葡萄糖摄取和利用，提示其可部分通过AMPK通路调节db/db小鼠的糖代谢。

     

    Abstract:
    ObjectiveTo 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.
    Methodsdb/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.
    ConclusionRosiglitazone 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.

     

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