Mitochondrial alteration in type 2 diabetes and obesity An epigenetic link

被引：69

作者：

Cheng, Zhiyong ^{[1
]}

Almeida, Fabio A. ^{[1
]}

机构：

[1] Virginia Tech, Dept Human Nutr Foods & Exercise, Fralin Translat Obes Res Ctr, Fralin Life Sci Inst,Coll Agr & Life Sci, Blacksburg, VA 24061 USA

来源：

CELL CYCLE | 2014年 / 13卷 / 06期

关键词：

mitochondrial alteration; epigenetic; type; 2; diabetes; obesity; lifestyle; HUMAN SKELETAL-MUSCLE; CANCER-FREE POPULATION; INDUCED INSULIN-RESISTANCE; GENOMIC DNA METHYLATION; FATTY-ACID OXIDATION; WEIGHT-LOSS; UNCOUPLING PROTEIN-2; PHYSICAL-ACTIVITY; GENE-EXPRESSION; BETA-CELLS;

D O I：

10.4161/cc.28189

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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 PGC1 alpha 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.

引用

页码：890 / 897

页数：8

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