CoChat
Sign Up
Cited by 243Tryptophan and brain disordersStress Responses and CortisolNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 84 of the 84 references it cites were found in a registry or an index.

Diet-induced obesity progressively alters cognition, anxiety-like behavior and lipopolysaccharide-induced depressive-like behavior: Focus on brain indoleamine 2,3-dioxygenase activation

André, Caroline, Dinel, Anne-Laure, Ferreira, Guillaume, Layé, Sophie, Castanon, Nathalie·2014·Brain Behavior and Immunity
DOI 10.1016/j.bbi.2014.03.012
Open this paper in CoChat — free account

Abstract

Obesity is associated with a high prevalence of mood symptoms and cognitive dysfunctions that emerges as significant risk factors for important health complications such as cardiovascular diseases and type 2 diabetes. It is therefore important to identify the dynamic of development and the pathophysiological mechanisms underlying these neuropsychiatric symptoms. Obesity is also associated with peripheral low-grade inflammation and increased susceptibility to immune-mediated diseases. Excessive production of proinflammatory cytokines and the resulting activation of the brain tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) have been shown to promote neurobehavioral complications, particularly depression. In that context, questions arise about the impact of diet-induced obesity on the onset of neuropsychiatric alterations and the increased susceptibility to immune-mediated diseases displayed by obese patients, particularly through brain IDO activation. To answer these questions, we used C57Bl/6 mice exposed to standard diet or western diet (WD; consisting of palatable energy-dense food) since weaning and for 20 weeks. We then measured inflammatory and behavioral responses to a systemic immune challenge with lipopolysaccharide (LPS) in experimental conditions known to alter cognitive and emotional behaviors independently of any motor impairment. We first showed that in absence of LPS, 9 weeks of WD is sufficient to impair spatial recognition memory (in the Y-maze). On the other hand, 18 weeks of WD increased anxiety-like behavior (in the elevated plus-maze), but did not affect depressive-like behavior (in the tail-suspension and forced-swim tests). However, 20 weeks of WD altered LPS-induced depressive-like behavior compared to LPS-treated lean mice and exacerbated hippocampal and hypothalamic proinflammatory cytokine expression and brain IDO activation. Taken together, these results show that WD exposure alters cognition and anxiety in unstimulated conditions and enhances activation of neurobiological mechanisms underlying depression after immune stimulation. They suggest therefore that obesity, and possibly obesity-associated inflammatory priming, may represent a vulnerability state to immune-mediated depressive symptoms.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.bbi.2014.03.012

Cites

84 of 84 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 84 references

Cited by

Sorted by citations

Items 101–200 of 243

Related

See all

Metadata

Authors
André, C., Dinel, A.-L., Ferreira, G., Layé, S., & Castanon, N.
Affiliations
Université de Bordeaux (FR)
Corresponding author
Castanon, Nathalie
ORCID
Venue
Brain Behavior and Immunity
Publisher
Elsevier BV
Published
2014-10
Volume
41
Pages
10-21
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2014.03.012
OpenAlex
W2034355214
Cited by
241
References
84
Citations by year
2026: 8 · 2025: 16 · 2024: 22 · 2023: 20 · 2022: 13 · 2021: 27 · 2020: 28 · 2019: 25 · 2018: 15 · 2017: 16 · 2016: 27 · 2015: 19 · 2014: 5
FWCI
6.87
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
diet-induced obesity, Western diet, indoleamine 2,3-dioxygenase, lipopolysaccharide, depression-like behavior, anxiety-like behavior, spatial recognition memory, inflammatory cytokines, neuroinflammation, hippocampus, hypothalamus, tryptophan metabolism, cognitive impairment
MeSH terms
Animals, Anxiety, Behavior, Animal, Brain, Cognition Disorders, Depression, Endotoxins, Enzyme Activation, Gene Expression Regulation, Hormones, Male, Memory Disorders, Mice, Inbred C57BL, Nerve Tissue Proteins, Obesity, Neuroimmunomodulation, Cytokines, Maze Learning, Indoleamine-Pyrrole 2,3,-Dioxygenase, Mice, Diet, Western

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review