Zhou Zheng, Sun Bao, Li Xiaoping, Zhu Chunsheng
1Department of Chinese Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000 China.
2Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410000 China.
Nutr Metab (Lond). 2018 Jun 28;15:47. doi: 10.1186/s12986-018-0283-x. eCollection 2018.
Although genetic variations and environmental factors are vital to the development and progression of type 2 diabetes mellitus (T2DM), emerging literature suggest that epigenetics, especially DNA methylation, play a key role in the pathogenesis of T2DM by affecting insulin secretion of pancreatic β cells and the body's resistance to insulin. Previous studies have elucidated how DNA methylation interacted with various factors in T2DM pathogenesis. This review summarized the role of related methylation genes in insulin-sensitive organs, such as pancreatic islets, skeletal muscle, liver, brain and adipose tissue, as well as peripheral blood cells, comparing the tissue similarity and specificity of methylated genes, aiming at a better understanding of the pathogenesis of T2DM and providing new ideas for the personalized treatment of this metabolism-associated disease.
尽管基因变异和环境因素对2型糖尿病(T2DM)的发生和发展至关重要,但新出现的文献表明,表观遗传学,尤其是DNA甲基化,通过影响胰腺β细胞的胰岛素分泌和机体对胰岛素的抵抗,在T2DM的发病机制中起关键作用。先前的研究已经阐明了DNA甲基化在T2DM发病机制中如何与各种因素相互作用。本综述总结了相关甲基化基因在胰岛素敏感器官,如胰岛、骨骼肌、肝脏、大脑和脂肪组织以及外周血细胞中的作用,比较了甲基化基因的组织相似性和特异性,旨在更好地理解T2DM的发病机制,并为这种代谢相关疾病的个性化治疗提供新思路。