Show simple item record

dc.contributor.authorHoulahan, Kathleen E.
dc.contributor.authorProkopec, Stephenie D.
dc.contributor.authorSun, Ren X.
dc.contributor.authorMoffat, Ivy D.
dc.contributor.authorLindén, Jere
dc.contributor.authorLensu, Sanna
dc.contributor.authorOkey, Allan B.
dc.contributor.authorPohjanvirta, Raimo
dc.contributor.authorBoutros, Paul C.
dc.date.accessioned2015-10-08T09:19:44Z
dc.date.available2015-10-08T09:19:44Z
dc.date.issued2015fi
dc.identifier.citationHoulahan, K., Prokopec, S., Sun, R., Moffat, I., Lindén, J., Lensu, S., . . . Boutros, P. (2015). Transcriptional profiling of rat white adipose tissue response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin. <em>Toxicology and Applied Pharmacology</em>, 288 (2), 223-231. <a href="http://dx.doi.org/10.1016/j.taap.2015.07.018">doi:10.1016/j.taap.2015.07.018</a>fi
dc.identifier.otherTUTKAID_66776
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/47279
dc.description.abstractPolychlorinated dibenzodioxins are environmental contaminants commonly produced as a by-product of industrial processes. The most potent of these, 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD), is highly lipophilic, leading to bioaccumulation. White adipose tissue (WAT) is a major site for energy storage, and is one of the organs in which TCDD accumulates. In laboratory animals, exposure to TCDD causes numerous metabolic abnormalities, including a wasting syndrome. We therefore investigated the molecular effects of TCDD exposure on WAT by profiling the transcriptomic response of WAT to 100 μg/kg of TCDD at 1 or 4 days in TCDD-sensitive Long-Evans (Turku/AB; L-E) rats. A comparative analysis was conducted simultaneously in identically treated TCDD-resistant Han/Wistar (Kuopio; H/W) rats one day after exposure to the same dose. We sought to identify transcriptomic changes coinciding with the onset of toxicity, while gaining additional insight into later responses. More transcriptional responses to TCDD were observed at 4 days than at 1 day post-exposure, suggesting WAT shows mostly secondary responses. Two classic AHR-regulated genes, Cyp1a1 and Nqo1, were significantly induced by TCDD in both strains, while several genes involved in the immune response, including Ms4a7 and F13a1 were altered in L-E rats alone. We compared genes affected by TCDD in rat WAT and human adipose cells, and observed little overlap. Interestingly, very few genes involved in lipid metabolism exhibited altered expression levels despite the pronounced lipid mobilization from peripheral fat pads by TCDD in L-E rats. Of these genes, the lipolysis-associated Lpin1 was induced slightly over 2-fold in L-E rat WAT on day 4.fi
dc.language.isoeng
dc.publisherAcademic Press
dc.relation.ispartofseriesToxicology and Applied Pharmacology
dc.subject.otherAHRfi
dc.subject.otherfeed restrictionfi
dc.subject.otherTCDDfi
dc.subject.othertranscriptomic profilingfi
dc.subject.otherwhite adipose tissuefi
dc.titleTranscriptional profiling of rat white adipose tissue response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxinfi
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-201510073315
dc.contributor.laitosLiikuntabiologian laitosfi
dc.contributor.laitosDepartment of Biology of Physical Activityen
dc.contributor.oppiaineLiikuntafysiologia
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.date.updated2015-10-07T06:15:04Z
dc.type.coarjournal article
dc.description.reviewstatuspeerReviewed
dc.format.pagerange223-231
dc.relation.issn0041-008X
dc.relation.volume288
dc.type.versionpublishedVersion
dc.rights.copyright© 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)
dc.rights.accesslevelopenAccessfi
dc.rights.urlhttp://creativecommons.org/licenses/by/4.0/
dc.relation.doi10.1016/j.taap.2015.07.018


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

© 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/)
Except where otherwise noted, this item's license is described as © 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)