Evidence map›Paper›PMID 27045846›Full record

ArticleTranslational psychiatry2016

BDNF-Val66Met variant and adolescent stress interact to promote susceptibility to anorexic behavior in mice.

M Madra, L M Zeltser

Abstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Animal Models for Anorexia Nervosa-A Systematic Review.Frontiers in human neuroscience · 2020
    Pooled it
  3. Recovery From Anorexia Nervosa: A Concept Analysis.Journal of advanced nursing · 2026
    Review
  4. Identification of a neural basis for anorexia nervosa.bioRxiv : the preprint server for biology · 2026
    Article
  5. Review
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  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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  15. Metabolic homeostasis via BDNF and its receptors.Trends in endocrinology and metabolism: TEM · 2021
    Review
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

M MadraInstitute of Human Nutrition, Columbia University, New York, NY, USA.
L M ZeltserNaomi Berrie Diabetes Center, Columbia University, New York, NY, USA.

Funding

Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DOMENICO ACCILI · 2003 to 2026
$36.7M
RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
Howard Hughes Medical InstituteNIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30 DK063608
6 · The paper itself

Abstract

There is an urgent need to identify therapeutic targets for anorexia nervosa (AN) because current medications do not impact eating behaviors that drive AN's high mortality rate. A major obstacle to developing new treatments is the lack of animal models that recapitulate the pattern of disease onset typically observed in human populations. Here we describe a translational mouse model to study interactions between genetic, psychological and biological risk factors that promote anorexic behavior. We combined several factors that are consistently associated with increased risk of AN-adolescent females, genetic predisposition to anxiety imposed by the BDNF-Val66Met gene variant, social isolation stress and caloric restriction (CR). Approximately 40% of the mice with all of these risk factors will exhibit severe self-imposed dietary restriction, sometimes to the point of death. We systematically varied the risk factors outlined above to explore how they interact to influence anorexic behavior. We found that the Val66Met genotype markedly increases the likelihood and severity of abnormal feeding behavior triggered by CR, but only when CR is imposed in the peri-pubertal period. Incidence of anorexic behavior in our model is dependent on juvenile exposure to social stress and can be extinguished by adolescent handling, but is discordant from anxiety-like behavior. Thus, this study characterized gene × environment interactions during adolescence that could be the underlying driver of abnormal eating behavior in certain AN patients, and represents a promising system to identify possible targets for therapeutic intervention.

Indexed as

Behavior, AnimalGene-Environment InteractionAnimalsAnorexia NervosaBrain-Derived Neurotrophic FactorCaloric RestrictionDisease Models, AnimalFeeding BehaviorFemaleGenetic Predisposition to DiseaseMethionineMicePolymorphism, Single NucleotideRisk FactorsSeverity of Illness IndexStress, PsychologicalBrain-Derived Neurotrophic FactorMethionineValine

Identifiers

PMID27045846
PMCPMC4872394

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.