Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
Ann N Y Acad Sci. 2010 Jul;1201:157-65. doi: 10.1111/j.1749-6632.2010.05625.x.
Abundant evidence has been accumulated to suggest that mitochondrial dysfunction is associated with type 2 diabetes. Research findings from this and other laboratories have supported the notion that impaired mitochondrial function is a cause of insulin insensitivity in myocytes and adipocytes as a result of insufficient supply of energy or defects in the insulin signaling pathway. We demonstrated that inhibition of respiration and oxidative phosphorylation by respiratory inhibitors or knockdown of genes involved in mitochondrial biogenesis can impair the differentiation of preadipocytes and response of adipocytes to insulin. Moreover, defective mitochondria also cause a decrease in adiponectin secretion that leads to decline glucose utilization of other tissues. Besides, it has been elucidated that some environmental factors, pollutants, and mitochondrial toxins are involved in the pathogenesis of type 2 diabetes. Taken together, we suggest that mitochondrial dysfunction plays a role in the pathophysiology of insulin insensitivity, and that activation of mitochondrial biogenesis may be an effective strategy in the prevention or treatment of insulin resistance and type 2 diabetes.
大量证据表明，线粒体功能障碍与 2 型糖尿病有关。本实验室和其他实验室的研究结果支持这样一种观点，即线粒体功能受损是肌细胞和脂肪细胞胰岛素敏感性降低的原因，这是由于能量供应不足或胰岛素信号通路缺陷所致。我们证明，呼吸抑制剂抑制呼吸和氧化磷酸化或敲低参与线粒体生物发生的基因，可损害前脂肪细胞的分化和脂肪细胞对胰岛素的反应。此外，功能失调的线粒体还会导致脂联素分泌减少，从而导致其他组织葡萄糖利用减少。此外，已经阐明一些环境因素、污染物和线粒体毒素参与了 2 型糖尿病的发病机制。综上所述，我们认为线粒体功能障碍在胰岛素抵抗的病理生理学中起作用，激活线粒体生物发生可能是预防或治疗胰岛素抵抗和 2 型糖尿病的有效策略。
