CAJ | 학술논문

线粒体是提供细胞进行各种生命活动所需能量的细胞器,越来越多的证据表明,线粒体功能与骨骼肌胰岛素抵抗状态密切相关,这种机制可能因为线粒体功能损伤引发脂肪酸β-氧化功能障碍,最终影响胰岛素受体后信号转导通路而致胰岛素抵抗的发生；也可因为线粒体融合蛋白或基因调控受损造成线粒体动力学异常或膜电位下降,造成胰岛素抵抗.目前对于线粒体功能障碍的研究,尤其是氧化应激机制的研究,可为治疗2型糖尿病提供新的思路.
선립체시제공세포진행각충생명활동소수능량적세포기,월래월다적증거표명,선립체공능여골격기이도소저항상태밀절상관,저충궤제가능인위선립체공능손상인발지방산β-양화공능장애,최종영향이도소수체후신호전도통로이치이도소저항적발생；야가인위선립체융합단백혹기인조공수손조성선립체동역학이상혹막전위하강,조성이도소저항.목전대우선립체공능장애적연구,우기시양화응격궤제적연구,가위치료2형당뇨병제공신적사로.
Mitochondria are the organelles which can provide energy to carry out various life activities.More and more evidences have shown that mitochondrial dysfunction is closely related to skeletal muscle insulin resistance.The mechanism may be the dysfunction of fatty acid beta oxidation,caused by the damage of mitochondria thus affecting insulin receptor signaling pathways,and finally resulting in the occurrence of insulin resistance.In addition,dysregulation of mitochondria fusion protein and gene expression can cause abnormal mitochondria dynamics or downregulation of membrane potential,finally leads to insulin resistance.The current research on mitochondrial dysfunction,especially oxidative stress will provide new ideas for the treatment of type 2 diabetes.