A Methyl-Balanced Diet Prevents CRF-Induced Prenatal Stress-Triggered Predisposition to Binge Eating-like Phenotype

被引:26
|
作者
Schroeder, Mariana [1 ,2 ]
Jakovcevski, Mira [2 ]
Polacheck, Tamar [1 ,2 ]
Lebow, Maya [1 ,2 ]
Drori, Yonat [1 ,2 ]
Engel, Mareen [2 ]
Ben-Dor, Shifra [3 ]
Chen, Alon [1 ,2 ]
机构
[1] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel
[2] Max Planck Inst Psychiat, Dept Stress Neurobiol & Neurogenet, D-80804 Munich, Germany
[3] Weizmann Inst Sci, Bioinformat & Biol Comp Unit, Biol Serv, IL-76100 Rehovot, Israel
基金
欧洲研究理事会; 以色列科学基金会;
关键词
DNA METHYLATION; MAMMALIAN-CELLS; CHILDHOOD ABUSE; GENE-EXPRESSION; SEX-DIFFERENCES; PAX-GENES; FETAL; MICE; DISORDERS; SUPPLEMENTATION;
D O I
10.1016/j.cmet.2017.05.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Binge eating (BE) is a common aberrant form of eating behavior, characterized by overconsumption of food in a brief period of time. Recurrent episodes of BE constitute the BE disorder, which mostly affects females and is associated with early-life adversities. Here, we show that corticotropin releasing factor (CRF)-induced prenatal stress (PNS) in late gestation predisposes female offspring to BE-like behavior that coincides with hypomethylation of hypothalamic miR-1a and downstream dysregulation of the melanocortin system through Pax7/Pax3. Moreover, exposing the offspring to a methyl-balanced diet during adolescence prevents the dysregulation and predisposition from being triggered. We demonstrate that gestational programming, per se, will not lead to BE-like behavior, but pre-existing alterations due to prenatal programming are revealed only when challenged during adolescence. We provide experimental evidence for long-term epigenetic abnormalities stemming from PNS in predisposing female offspring to BE disorder as well as a potential non-invasive prevention strategy.
引用
收藏
页码:1269 / +
页数:19
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