PNAS:南大陈帅课题组发表肥胖发病机理研究成果

2016-06-21 南京大学模式动物研究所 陈帅 PNAS


    AMPK-TBC1D1-Rab8a-IGF-1通路在体内能量状态感知与肥胖发生中作用机制示意图

南京大学模式动物研究所陈帅教授实验室在肥胖发病机理研究中取得重要进展,相关成果“Disruption of the AMPK–TBC1D1 nexus increases lipogenic gene expression and causes obesity in mice via promoting IGF1 secretion”于2016年6月15日在线发表在《美国科学院院报》(PNAS)。南京大学博士研究生陈亮、陈俏利和谢冰弦为论文共同第一作者,陈帅教授和王宏宇副研究员为共同通讯作者。

生活方式和饮食结构的改变导致近年来我国肥胖发病率急剧增加,而肥胖是诱发糖尿病、脂肪肝、高血压、心脑血管疾病等许多慢性病的重要危险因素。缺乏运动以及高能量食物摄入会改变身体内能量状态,最终导致肥胖,但这背后的分子机制尚不完全清楚。

该论文利用细胞生物学和生物化学方法结合基因工程小鼠模型,对能量过剩导致肥胖的分子机制进行了系统研究。腺苷酸激活的蛋白激酶(AMPK)是细胞的能量感受器:能量过剩时如缺乏运动或过多能量摄入,AMPK活性会被抑制;而能量缺乏时,AMPK会被激活。本文作者发现AMPK激活可抑制细胞分泌胰岛素样生长因子-1(IGF-1)。其机制是AMPK磷酸化RabGAP蛋白TBC1D1上的丝氨酸231位点(Ser231),抑制其GAP活性,从而减少下游分子开关Rab8a的GDP装载形式;而GDP装载的Rab8a可以促进细胞分泌IGF-1。当在小鼠体内利用基因工程手段将TBC1D1上231位的丝氨酸突变为非磷酸化的丙氨酸时,IGF-1分泌增加致使小鼠中IGF1R-PKB-mTOR通路活化,进而促进生长和脂质合成,导致小鼠罹患肥胖;而肥胖又进一步致使TBC1D1Ser231Ala基因敲入小鼠发生糖尿病和脂肪肝。该研究阐明了AMPK-TBC1D1-Rab8a-IGF-1通路在体内能量状态感知与肥胖发生中的作用机制,为今后干预和治疗肥胖提供了新靶点和新思路。

原始出处

Liang Chena,1, Qiaoli Chena,1, Bingxian Xiea,1, Chao Quana, Yang Shenga, Sangsang Zhua, Ping Ronga, Shuilian Zhoua, Kei Sakamotob, Carol MacKintoshc, Hong Yu Wanga,d,2,3, and Shuai Chena,d,2,3.Disruption of the AMPK–TBC1D1 nexus increases lipogenic gene expression and causes obesity in mice via promoting IGF1 secretion.PNAS.2016

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    2017-01-24 drwjr
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    2016-09-21 1e10c84am36(暂无匿称)

    文章很好,非常有益

    0

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    2016-09-21 1e10c84am36(暂无匿称)

    文章很好,非常有益

    0

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    2016-09-13 舒心和人

    新通路的发现对疾病的治疗提供了更有针对性的靶点,学习新知识了,感谢

    0

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