Publication date: Available online 30 May 2017
Source:Cell Metabolism
Author(s): Mariana Schroeder, Mira Jakovcevski, Tamar Polacheck, Maya Lebow, Yonat Drori, Mareen Engel, Shifra Ben-Dor, Alon Chen
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.
Graphical abstract
Teaser
Binge eating seems to mostly affect females. Schroeder et al. show that that late gestation prenatal stress rewires neural circuits in female mice, leading to binge-like behavior, if triggered during adolescence. Remarkably, this predisposition to binge eating can be prevented by a balanced, methyl-rich diet.http://ift.tt/2sm0d33
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου