Abstract
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.
Original language | English |
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Pages (from-to) | 1269-1281.e6 |
Journal | Cell Metabolism |
Volume | 25 |
Issue number | 6 |
DOIs | |
State | Published - 6 Jun 2017 |
Keywords
- CRF
- binge eating
- developmental origin of disease hypothesis
- developmental programming
- dietary manipulations
- early-life adversities
- eating behavior
- eating disorder
- methyl balanced diet
- prenatal stress
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Physiology
- Cell Biology