Mitochondrial alteration in type 2 diabetes and obesity: an epigenetic link.

Mitochondrial alteration in type 2 diabetes and obesity: an epigenetic link.
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DOI:
10.4161/cc.28189
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发表时间:
2014
期刊:
Cell cycle (Georgetown, Tex.)
影响因子:
--
通讯作者:
Almeida FA
Almeida FA
中科院分区:
其他
文献类型:
--
作者:
Cheng Z;Almeida FA

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2型糖尿病(T2 DM)和肥胖症的流行在很大程度上归因于目前过度消费和缺乏体育活动的生活方式。线粒体作为控制代谢和能量动态平衡的主要平台,在2型糖尿病和肥胖者中表现出异常变化。虽然潜在的机制正在进行广泛的研究,但表观遗传调节现在正在出现,在线粒体的生物发生、功能和动力学中发挥重要作用。在改变生活方式以防止线粒体改变和代谢紊乱的同时,运动已被证明改变了pGC1DNA启动子的α甲基化,有利于参与线粒体生物发生和功能的基因表达。本文讨论了T2 DM和肥胖症患者线粒体改变的表观遗传学机制,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表观遗传机制并将其与生活方式改变相结合的研究可能会导致针对线粒体改变和代谢紊乱的跨学科干预和新的预防选择。
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.
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