Department of Human Nutrition, Foods, and Exercise; Fralin Translational Obesity Research Center; Fralin Life Science Institute; College of Agriculture and Life Sciences; Virginia Tech; Blacksburg, VA USA.
Cell Cycle. 2014;13(6):890-7. doi: 10.4161/cc.28189. Epub 2014 Feb 12.
The growing epidemic of type 2 diabetes mellitus (T2DM) and obesity is largely attributed to the current lifestyle of over-consumption and physical inactivity. As the primary platform controlling metabolic and energy homeostasis, mitochondria show aberrant changes in T2DM and obese subjects. While the underlying mechanism is under extensive investigation, epigenetic regulation is now emerging to play an important role in mitochondrial biogenesis, function, and dynamics. In line with lifestyle modifications preventing mitochondrial alterations and metabolic disorders, exercise has been shown to change DNA methylation of the promoter of PGC1α to favor gene expression responsible for mitochondrial biogenesis and function. In this article we discuss the epigenetic mechanism of mitochondrial alteration in T2DM and obesity, and the effects of lifestyle on epigenetic regulation. Future studies designed to further explore and integrate the epigenetic mechanisms with lifestyle modification may lead to interdisciplinary interventions and novel preventive options for mitochondrial alteration and metabolic disorders.
2 型糖尿病(T2DM)和肥胖症的发病率不断上升,主要归因于目前过度饮食和缺乏身体活动的生活方式。线粒体作为控制代谢和能量平衡的主要平台,在 T2DM 和肥胖患者中表现出异常变化。虽然其潜在机制正在广泛研究中,但表观遗传调控现已成为影响线粒体生物发生、功能和动力学的重要因素。与预防线粒体改变和代谢紊乱的生活方式改变一致,运动已被证明可以改变 PGC1α 启动子的 DNA 甲基化,有利于负责线粒体生物发生和功能的基因表达。本文讨论了 T2DM 和肥胖症中线粒体改变的表观遗传机制,以及生活方式对表观遗传调控的影响。未来旨在进一步探索和整合表观遗传机制与生活方式改变的研究,可能为线粒体改变和代谢紊乱提供跨学科干预和新的预防选择。