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迷失基因激活蛋白激酶酸-5在患有1型和2型糖尿病的小鼠中加剧了岛屿功能障碍

Tongjian Zhao¹, Yafei Tian¹, Jianan Zhao¹

¹School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin, China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|February 2, 2024

概括

缺乏基因激活蛋白激酶酸酶-5 (MKP-5) 的小鼠显示糖尿病症状恶化. MKP-5的淘汰会损害细胞自和增加岛屿细胞内质网膜应激,这表明MKP-5对糖尿病管理至关重要.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

岛屿β细胞功能障碍是1型和2型糖尿病 (T1DM和T2DM) 的核心.
在糖尿病病变发生过程中,内源性线粒激活蛋白激酶酸酶-5 (MKP-5) 的作用尚不清楚.
以前的研究表明外源MKP-5会影响与肥胖相关的T2DM.

研究的目的:

研究内源MKP-5在T1DM和T2DM中的作用.
在MKP-5淘汰赛 (KO) 模型中阐明小岛功能障碍的分子机制.
探索细胞内膜网膜应激 (ERS) 和自在MKP-5缺乏的T2DM中的参与.

主要方法:

产生MKP-5淘汰赛 (KO) 的小鼠.
使用KO小鼠建立了T1DM和T2DM的小鼠模型.
在T2DM KO小鼠的小岛上进行RNA测序,以分析ERS和自途径.

主要成果:

在T1DM和T2DM模型中,MKP-5KO小鼠表现出恶化的糖尿病症状.
T2DM MKP-5 KO岛屿显示自性受损和ERS增加.
RNA测序揭示了5'腺单酸激活蛋白激酶 (AMPK) 介导的自抑制和T2DMKO岛屿中的葡萄糖调节蛋白78 (GRP-78) 驱动的ERS.

结论:

内源MKP-5在糖尿病中起着保护作用.
由GRP-78介导的自性损伤,有助于MKP-5缺乏T2DM的岛屿功能障碍.
向MKP-5可能为糖尿病管理提供新的治疗策略.

关键词:

这就是AMPKK.在GRP-78中使用.在MKP-5中,MKP-5是MKP-5.在糖尿病中,糖尿病是血糖类的.小岛的功能障碍.序列分析分析的序列分析.

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