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NYGGF4(PID1)过表达导致 3T3-L1 脂肪细胞线粒体损伤。

Overexpression of NYGGF4 (PID1) induces mitochondrial impairment in 3T3-L1 adipocytes.

机构信息

Department of Endocrinology, The 82nd Hospital of the People's Liberation Army, No. 100 Jiankang East Road, 223001 Huaian, China.

出版信息

Mol Cell Biochem. 2010 Jul;340(1-2):41-8. doi: 10.1007/s11010-010-0398-5. Epub 2010 Feb 18.

Abstract

NYGGF4 is a recently discovered gene that is involved in obesity-associated insulin resistance. The exact mechanism by which NYGGF4 induces insulin resistance has not yet been fully elucidated. In this study, we demonstrated that the overexpression of NYGGF4 in 3T3-L1 adipocytes decreased mitochondrial mass, mitochondrial DNA, and intracellular ATP synthesis. In addition, NYGGF4 overexpression also led to an imbalance of the mitochondrial dynamics and excess intracellular ROS production. Collectively, our results indicated that the overexpression of NYGGF4 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of NYGGF4-induced insulin resistance.

摘要

NYGGF4 是最近发现的一个与肥胖相关的胰岛素抵抗有关的基因。NYGGF4 诱导胰岛素抵抗的确切机制尚未完全阐明。在这项研究中,我们证明了 3T3-L1 脂肪细胞中 NYGGF4 的过表达会降低线粒体质量、线粒体 DNA 和细胞内 ATP 合成。此外,NYGGF4 的过表达还导致线粒体动力学失衡和过量的细胞内 ROS 产生。总之,我们的结果表明,NYGGF4 的过表达导致脂肪细胞中线粒体功能障碍,这可能是 NYGGF4 诱导胰岛素抵抗的原因。

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