Epigenetic mechanisms in the development of type 2 diabetes

被引：131

作者：

Pinney, Sara E.

Simmons, Rebecca A. ^{[1
]}

机构：

[1] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2010年 / 21卷 / 04期

基金：

美国国家卫生研究院;

关键词：

INTRAUTERINE GROWTH-RETARDATION; IMPAIRED GLUCOSE-TOLERANCE; BETA-CELL MASS; DNA METHYLATION; OXIDATIVE STRESS; CHROMATIN-STRUCTURE; INSULIN-SECRETION; HOMEOBOX GENE; MOUSE EMBRYO; HISTONE H3;

D O I：

10.1016/j.tem.2009.10.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Type 2 diabetes (T2D) is a disorder of complex genetics influenced by interactions between susceptible genetic loci and environmental perturbations. Intrauterine growth retardation is one such environmental perturbation linked to the development of T2D in adulthood. An abnormal metabolic intrauterine milieu affects fetal development by permanently modifying expression of key genes regulating beta-cell development (Pdx1) and glucose transport (Glut4) in muscle. Epigenetic regulation of gene expression is one mechanism by which genetic susceptibility and environmental insults can lead to T2D. Therefore, therapeutic agents targeting epigenetic gene regulation can ultimately be used to treat T2D; however, there is much to be learned about genome-wide epigenetic programming of health and disease before these therapies can be used in patient care.

引用

页码：223 / 229

页数：7