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The Disruptive Effects of Estrogen Removal before Puberty on Risk for Binge Eating in Female Rats.

ABSTRACT: Recent research suggests that estrogen is protective against binge eating in adult females, and that pubertal estrogen may be critical for these effects. Nonetheless, to date, no study has examined the role of pubertal estrogen in adult binge eating phenotypes in females, potentially due to difficulties experimentally manipulating estrogen in humans to examine causal effects. We used a novel animal model to examine whether estrogen removal prior to puberty (via pre-pubertal ovariectomy (P-OVX)) increases rates of binge eating prone (BEP) phenotypes in adulthood in females. A total of 77 P-OVX and 79 intact rats were followed from pre-puberty into adulthood and phenotyped for BEP status in adulthood. Results showed significantly increased rates (~2-8x higher) of adult BEP phenotypes in P-OVX as compared to intact rats. Findings confirm that estrogen removal substantially increases later risk for binge eating in females, potentially by disrupting typical adolescent brain development.

SUBMITTER: Klump KL

PROVIDER: S-EPMC7983810 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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The Disruptive Effects of Estrogen Removal before Puberty on Risk for Binge Eating in Female Rats.

Klump Kelly L KL Sinclair Elaine B EB Hildebrandt Britny A BA Kashy Deborah A DA O'Connor Shannon S Mikhail Megan E ME Culbert Kristen M KM Johnson Alexander A Sisk Cheryl L CL

Clinical psychological science : a journal of the Association for Psychological Science 20200702 5

Recent research suggests that estrogen is protective against binge eating in adult females, and that pubertal estrogen may be critical for these effects. Nonetheless, to date, no study has examined the role of pubertal estrogen in adult binge eating phenotypes in females, potentially due to difficulties experimentally manipulating estrogen in humans to examine causal effects. We used a novel animal model to examine whether estrogen removal prior to puberty (via pre-pubertal ovariectomy (P-OVX)) ...[more]

PMID: 33758686

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Project description:Binge eating disorder (BED) is the most frequent eating disorder, for which current pharmacotherapies show poor response rates and safety concerns, thus highlighting the need for novel treatment options. The lipid-derived messenger oleoylethanolamide (OEA) acts as a satiety signal inhibiting food intake through the involvement of central noradrenergic and oxytocinergic neurons. We investigated the anti-binge effects of OEA in a rat model of binge-like eating, in which, after cycles of intermittent food restrictions/refeeding and palatable food consumptions, female rats show a binge-like intake of palatable food, following a 15-min exposure to their sight and smell ("frustration stress"). Systemically administered OEA dose-dependently (2.5, 5, and 10 mg kg-1) prevented binge-like eating. This behavioral effect was associated with a decreased activation (measured by mapping the expression of c-fos, an early gene widely used as a marker of cellular activation) of brain areas responding to stress (such as the nucleus accumbens and amygdala) and to a stimulation of areas involved in the control of food intake, such as the VTA and the PVN. These effects were paralleled, also, to the modulation of monoamine transmission in key brain areas involved in both homeostatic and hedonic control of eating. In particular, a decreased dopaminergic response to stress was observed by measuring dopamine extracellular concentrations in microdialysates from the nucleus accumbens shell, whereas an increased serotonergic and noradrenergic tone was detected in tissue homogenates of selected brain areas. Finally, a decrease in corticotropin-releasing factor (CRF) mRNA levels was induced by OEA in the central amygdala, while an increase in oxytocin mRNA levels was induced in the PVN. The restoration of a normal oxytocin receptor density in the striatum paralleled the oxytocinergic stimulation produced by OEA. In conclusion, we provide evidence suggesting that OEA might represent a novel potential pharmacological target for the treatment of binge-like eating behavior.

Project description:The heritability of eating disorder (ED) symptoms increases dramatically across gonadarche in girls. Past studies suggest these developmental differences could be due to pubertal activation of estrogen, but findings have been limited to only one ED symptom (i.e., binge eating). The current study examined whether estrogen contributes to gonadarcheal differences in genetic influences on overall levels of ED symptoms as well as key cognitive symptoms (i.e., weight/shape concerns) that are present across all EDs and are early risk factors for eating pathology. Given that binge eating frequently co-occurs with all of these symptoms, analyses also examined whether estrogen effects exist for overall levels of ED symptoms and body weight/shape concerns after accounting for the known effects of estrogen on genetic risk for binge eating. Participants included 964 female twins (ages 8-16) from the Michigan State University Twin Registry. Overall levels of ED symptoms were assessed with the Minnesota Eating Behavior Survey (MEBS) total score. Weight/shape concerns were assessed with a latent factor modeled using subscales from the MEBS and the Eating Disorder Examination Questionnaire. Estradiol levels were assessed with saliva samples. Twin moderation models were used to examine whether genetic influences on overall levels of ED symptoms and weight/shape concerns differed significantly across estradiol levels. Although initial models suggested modest differences in genetic influences on overall levels of ED symptoms across estradiol levels, these effects were eliminated when binge eating was accounted for in the models. In addition, weight/shape concerns did not show significant moderation of genetic influences by estradiol in models with or without binge eating. Taken together, results are significant in suggesting that individual differences in estradiol levels during gonadarche have a unique and specific impact on genetic risk for binge eating, while other etiologic factors must contribute to increased heritability of cognitive ED symptoms during this key developmental period in girls.

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The Disruptive Effects of Estrogen Removal before Puberty on Risk for Binge Eating in Female Rats.

Publications

The Disruptive Effects of Estrogen Removal before Puberty on Risk for Binge Eating in Female Rats.

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