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Adipose tissue dysfunction as a central mechanism leading to dysmetabolic obesity triggered by chronic exposure to p,p’-DDE

2017Journal article Open access
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dc.contributor.authorPestana, Diogo
dc.contributor.authorTeixeira, Diana
dc.contributor.authorMeireles, Manuela
dc.contributor.authorMarques, Cláudia
dc.contributor.authorNorberto, Sónia
dc.contributor.authorSá, Carla
dc.contributor.authorFernandes, Virgínia
dc.contributor.authorCorreia-Sá, Luísa
dc.contributor.authorFaria, Ana
dc.contributor.authorGuardão, Luísa
dc.contributor.authorGuimarães, João T.
dc.contributor.authorCooper, Wendy N.
dc.contributor.authorSandovici, Ionel
dc.contributor.authorDomingues, Valentina
dc.contributor.authorDelerue-Matos, Cristina
dc.contributor.authorMonteiro, Rosário
dc.contributor.authorConstância, Miguel
dc.contributor.authorCalhau, Conceição
dc.date.accessioned2019-06-06T13:50:54Z
dc.date.available2019-06-06T13:50:54Z
dc.date.issued2017
dc.description.abstractEndocrine-disrupting chemicals such as p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), are bioaccumulated in the adipose tissue (AT) and have been implicated in the obesity and diabetes epidemic. Thus, it is hypothesized that p,p'-DDE exposure could aggravate the harm of an obesogenic context. We explored the effects of 12 weeks exposure in male Wistar rats' metabolism and AT biology, assessing a range of metabolic, biochemical and histological parameters. p,p'-DDE -treatment exacerbated several of the metabolic syndrome-accompanying features induced by high-fat diet (HF), such as dyslipidaemia, glucose intolerance and hypertension. A transcriptome analysis comparing mesenteric visceral AT (vAT) of HF and HF/DDE groups revealed a decrease in expression of nervous system and tissue development-related genes, with special relevance for the neuropeptide galanin that also revealed DNA methylation changes at its promoter region. Additionally, we observed an increase in transcription of dipeptidylpeptidase 4, as well as a plasmatic increase of the pro-inflammatory cytokine IL-1β. Our results suggest that p,p'-DDE impairs vAT normal function and effectively decreases the dynamic response to energy surplus. We conclude that p,p'-DDE does not merely accumulate in fat, but may contribute significantly to the development of metabolic dysfunction and inflammation. Our findings reinforce their recognition as metabolism disrupting chemicals, even in non-obesogenic contexts.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1038/s41598-017-02885-9pt_PT
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/10400.22/13878
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relation.publisherversionhttps://www.nature.com/articles/s41598-017-02885-9pt_PT
dc.subjectp,p’-DDEpt_PT
dc.subjectAdipose tissue (AT)pt_PT
dc.titleAdipose tissue dysfunction as a central mechanism leading to dysmetabolic obesity triggered by chronic exposure to p,p’-DDEpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue1pt_PT
oaire.citation.startPage2738pt_PT
oaire.citation.titleScientific Reportspt_PT
oaire.citation.volume7pt_PT
person.familyNameFernandes
person.familyNameCorreia-Sá
person.familyNameDomingues
person.familyNameDelerue-Matos
person.givenNameVirgínia
person.givenNameLuísa
person.givenNameValentina Maria Fernandes
person.givenNameCristina
person.identifier.ciencia-id5A16-3713-E0CE
person.identifier.ciencia-id231E-E28E-94D9
person.identifier.ciencia-id4E16-791D-6664
person.identifier.ciencia-id9A1A-43FB-5C27
person.identifier.orcid0000-0003-3979-7523
person.identifier.orcid0000-0003-1135-0260
person.identifier.orcid0000-0003-3472-849X
person.identifier.orcid0000-0002-3924-776X
person.identifier.ridG-4985-2010
person.identifier.ridQ-5259-2018
person.identifier.ridD-4990-2013
person.identifier.scopus-author-id37045954500
person.identifier.scopus-author-id55070939500
person.identifier.scopus-author-id6603741848
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicatione30d74c3-1a3a-4e3e-ada0-5e79362cdd6e
relation.isAuthorOfPublicatione5b2f84a-6e8c-49ce-a7ee-d9dcccf2fb6e
relation.isAuthorOfPublicationbe653ab6-34ec-4329-972a-eee990a7ec66
relation.isAuthorOfPublication09f6a7bd-2f15-42b0-adc5-04bd22210519
relation.isAuthorOfPublication.latestForDiscoverybe653ab6-34ec-4329-972a-eee990a7ec66

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