中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (25): 2379-2388.doi: 10.3969/j.issn.1673-5374.2013.25.009

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

二甲双胍抑制食物的摄入和下丘脑神经肽Y基因的表达

  

  • 收稿日期:2013-05-27 修回日期:2013-08-06 出版日期:2013-09-05 发布日期:2013-09-05

Metformin inhibits food intake and neuropeptide Y gene expression in the hypothalamus

Yale Duan1, Rui Zhang1, Min Zhang2, Lijuan Sun1, Suzhen Dong1, Gang Wang2, Jun Zhang2, Zheng Zhao1   

  1. 1 Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, Shanghai 200062, China

    2 Department of Clinical Laboratory, Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China
  • Received:2013-05-27 Revised:2013-08-06 Online:2013-09-05 Published:2013-09-05
  • Contact: Jun Zhang, Ph.D., Associate professor, Master’s supervisor, Department of Clinical Laboratory, Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China, zhangjun@shaphc.org. Zheng Zhao, Ph.D., Professor, Doctoral supervisor, Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, Shanghai 200062, China, zzhao@brain.ecnu. edu.cn
  • About author:Yale Duan, Master.

摘要:

二甲双胍被广泛用于治疗2型糖尿病。 它也有许多健康益处,尤其是通过降低代谢综合征的相关风险。然而,在这方面,二甲双胍在中枢神经系统中的作用仍然知之甚少。这项研究调查二甲双胍的中枢作用,和探索这种药物在大鼠下丘脑的作用的可能机制。二甲双胍单侧脑室给药后3h,大鼠从脑室给药compound C。我们发现,二甲双胍中枢给药显著减少食物摄入量和体质量增长,尤其是在给药后4 h后。相应地,给药后4h,神经肽Y的表达减少了,诱导了下丘脑中的AMPK磷酸化,这些可以被compound C抑制,它是常用二甲双胍的AMPK拮抗剂。二甲双胍可以通过降低血浆低密度脂蛋白胆固醇改善脂质代谢。我们的研究表明,在正常的生理条件下二甲双胍可以抑制神经肽Y基因的表达,激活AMPK可能只是二甲双胍减食欲效应一个响应。

关键词: 神经再生, 脑损伤;二甲双胍, 食物的摄入量, 体重增加, 下丘脑, AMPK, NPY, 基金资助文章

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