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

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dc.citation.volume59
dc.contributor.authorRodrigues, Maria Elizabeth de Sousa [UNIFESP]
dc.contributor.authorBekhbat, Mandakh
dc.contributor.authorHouser, Madelyn C.
dc.contributor.authorChang, Jianjun
dc.contributor.authorWalker, Douglas I.
dc.contributor.authorJones, Dean P.
dc.contributor.authorNascimento, Claudia Maria da Penha Oller do [UNIFESP]
dc.contributor.authorBarnum, Christopher J.
dc.contributor.authorTansey, Malu G.
dc.coverageSan Diego
dc.date.accessioned2020-07-31T12:47:00Z
dc.date.available2020-07-31T12:47:00Z
dc.date.issued2017
dc.description.abstractThe 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. C57BI/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. (C) 2016 Elsevier Inc. All rights reserved.en
dc.description.affiliationEmory Univ, Sch Med, Dept Physiol, 605L Whitehead Biomed Res Bldg,615 Michael St, Atlanta, GA 30322 USA
dc.description.affiliationEmory Univ, Sch Med, Div Pulm Allergy & Crit Care Med, Atlanta, GA USA
dc.description.affiliationUniv Fed Sao Paulo, Dept Physiol Nutr, Sao Paulo, SP, Brazil
dc.description.affiliationEmory Univ, Sch Med, Div Pulm Allergy & Crit Care Med, Clin Biomarkers Lab, Whitehead Biomed Res Bldg,Room 225, Atlanta, GA USA
dc.description.affiliationUniv Fed Sao Paulo, Dept Fisiol, Disciplina Fisiol Nutr, Edificio Ciencias Biomed,Rua Botucatu 862, BR-04023060 Sao Paulo, SP, Brazil
dc.description.affiliationUnifespDepartamento de Fisiologia, Disciplina de Fisiologia da Nutrição, Universidade Federal de São Paulo, Edifício de Ciências Biomédicas, Rua Botucatu 862, Vila Clementino, 04023060 São Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipEmory Multiplexed Immunoassay Core (EMIC)
dc.description.sponsorshipEmory University School of Medicine
dc.description.sponsorshipNational Center for Advancing Translational Sciences of the National Institutes of Health
dc.description.sponsorshipNational Institutes of Health (NIH)/National Institute of Mental Health (NIMH)
dc.description.sponsorshipIDNational Center for Advancing Translational Sciences of the National Institutes of Health: UL1TR000454
dc.description.sponsorshipIDNIH/NIMHS: 1R43MH105048-01A1
dc.format.extent158-172
dc.identifierhttp://dx.doi.org/10.1016/j.bbi.2016.08.021
dc.identifier.citationBrain Behavior And Immunity. San Diego, v. 59, p. 158-172, 2017.
dc.identifier.doi10.1016/j.bbi.2016.08.021
dc.identifier.issn0889-1591
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/56512
dc.identifier.wosWOS:000390618700016
dc.language.isoeng
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofBrain Behavior And Immunity
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectPredatory stressen
dc.subjectDepressionen
dc.subjectMetabolic syndromeen
dc.subjectInsulinen
dc.subjectCholesterolen
dc.subjectLipocalin-2en
dc.subjectMetabolomicsen
dc.subjectBiliverdinen
dc.titleChronic 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 miceen
dc.typeinfo:eu-repo/semantics/article
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