Evidence map›Paper›PMID 27592562›Full record

ArticleBrain, behavior, and immunity2017

Chronic psychological stress and high-fat high-fructose diet disrupt metabolic and inflammatory gene networks in the brain, liver, and gut and promote behavioral deficits in mice.

Maria Elizabeth de Sousa Rodrigues, Mandakh Bekhbat, Madelyn C Houser, Jianjun Chang, Douglas I Walker, Dean P Jones, Claudia M P Oller do Nascimento, Christopher J Barnum, Malú G Tansey

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
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

56 citing papers in PubMed, 127 citations in OpenAlex.

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  5. Lack of GPNMB Is Associated With Altered Lipid and Glucose Metabolism and Disrupted Diurnal Hepatic Glycogen Regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Journal of diabetes and metabolic disorders · 2025
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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

9 authors at 2 institutions in 2 countries.

Maria Elizabeth de Sousa RodriguesDepartment of Physiology, School of Medicine at Emory University, United States; Department of Physiology of Nutrition, Federal University of Sao Paulo, SP, Brazil. Electronic address: mdesou2@emory.edu.
Mandakh BekhbatDepartment of Physiology, School of Medicine at Emory University, United States. Electronic address: mandakh.bekhbat@emory.edu.
Madelyn C HouserDepartment of Physiology, School of Medicine at Emory University, United States. Electronic address: mcrawf4@emory.edu.
Jianjun ChangDepartment of Physiology, School of Medicine at Emory University, United States. Electronic address: jchan47@emory.edu.
Douglas I WalkerDivision of Pulmonary, Allergy and Critical Care Medicine, School of Medicine at Emory University, United States. Electronic address: Douglas.Walker@emory.edu.
Dean P JonesDivision of Pulmonary, Allergy and Critical Care Medicine, School of Medicine at Emory University, United States. Electronic address: dpjones@emory.edu.
Claudia M P Oller do NascimentoDepartment of Physiology of Nutrition, Federal University of Sao Paulo, SP, Brazil. Electronic address: claudia.oller@unifesp.br.
Christopher J BarnumDepartment of Physiology, School of Medicine at Emory University, United States. Electronic address: cjbarnum@me.com.
Malú G TanseyDepartment of Physiology, School of Medicine at Emory University, United States. Electronic address: malu.tansey@emory.edu.
Emory University · USUniversidade Federal de São Paulo · BR

Funding

Implementing a Maternal health and PRegnancy Outcomes Vision for Everyone (IMPROVE)UL1TR002378 · NCATS · EMORY UNIVERSITY · PI Andres J Garcia, Elizabeth O. Ofili · 2017 to 2026
$92.1M
Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
Inflammation and Renin-Angiotensin System Dysfunction as risk factors for ADRF1AG051514 · NIA · EMORY UNIVERSITY · PI NORRIS, CHRISTOPHER MARK, WALKER, LARY C · 2015 to 2017
$3.6M
Orbitrap Elite/H-ESI BundleS10OD018006 · OD · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2014 to 2014
$600k
Novel Dominant Negative TNF Inhibitors for Treatment of DepressionR43MH105048 · NIMH · FPRT BIO, INC. · PI TANSEY, MARIA DE LOURDES GAMEZ, TESI, RAYMOND · 2015 to 2015
$350k
NCATS NIH HHS UL1 TR000454NCATS NIH HHS UL1 TR002378NIA NIH HHS RF1 AG051514NIH HHS S10 OD018006NIMH NIH HHS R43 MH105048
6 · The paper itself

Abstract

The mechanisms underlying the association between chronic psychological stress, development of metabolic syndrome (MetS), and behavioral impairment in obesity are poorly understood. The aim of the present study was to assess the effects of mild chronic psychological stress on metabolic, inflammatory, and behavioral profiles in a mouse model of diet-induced obesity. We hypothesized that (1) high-fat high-fructose diet (HFHF) and psychological stress would synergize to mediate the impact of inflammation on the central nervous system in the presence of behavioral dysfunction, and that (2) HFHF and stress interactions would impact insulin and lipid metabolism. C57Bl/6 male mice underwent a combination of HFHF and two weeks of chronic psychological stress. MetS-related conditions were assessed using untargeted plasma metabolomics, and structural and immune changes in the gut and liver were evaluated. Inflammation was measured in plasma, liver, gut, and brain. Our results show a complex interplay of diet and stress on gut alterations, energetic homeostasis, lipid metabolism, and plasma insulin levels. Psychological stress and HFHF diet promoted changes in intestinal tight junctions proteins and increases in insulin resistance and plasma cholesterol, and impacted the RNA expression of inflammatory factors in the hippocampus. Stress promoted an adaptive anti-inflammatory profile in the hippocampus that was abolished by diet treatment. HFHF increased hippocampal and hepatic Lcn2 mRNA expression as well as LCN2 plasma levels. Behavioral changes were associated with HFHF and stress. Collectively, these results suggest that diet and stress as pervasive factors exacerbate MetS-related conditions through an inflammatory mechanism that ultimately can impact behavior. This rodent model may prove useful for identification of possible biomarkers and therapeutic targets to treat metabolic syndrome and mood disorders.

Indexed as

AnimalsBehavior, AnimalBody WeightBrain ChemistryDiet, High-FatEnergy MetabolismFructoseGastrointestinal TractGene Regulatory NetworksInflammationLipid MetabolismLipocalin-2LiverMaleMetabolismMiceFructoseLcn2 protein, mouseLipocalin-2BiliverdinCholesterolDepressionInsulinLipocalin-2Metabolic syndromeMetabolomicsPredatory stress

Identifiers

PMID27592562
PMCPMC5154856
OpenAlexW2517479041

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.