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dc.contributor.authorHoulahan, Kathleen E.
dc.contributor.authorProkopec, Stephenie D.
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.accessioned2015-09-08T05:54:38Z
dc.date.available2015-09-08T05:54:38Z
dc.date.issued2015
dc.identifier.citationHoulahan, K., Prokopec, S., Moffat, I., Lindén, J., Lensu, S., Okey, A., . . . , & Boutros, P. (2015). Transcriptional profiling of rat hypothalamus response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin. <em>Toxicology</em>, 328 (3 February 2015), 93-101. <a href="http://dx.doi.org/10.1016/j.tox.2014.12.016">doi:10.1016/j.tox.2014.12.016</a>
dc.identifier.otherTUTKAID_64697
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/46788
dc.description.abstractIn some mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as significant weight loss associated with lethal outcomes. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR). Since TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, it was hypothesized that wasting syndrome is a result of to TCDD-induced dysregulation of genes involved in regulation of food-intake. As the hypothalamus is the central nervous systems' regulatory center for food-intake and energy balance. Therefore, mRNA abundances in hypothalamic tissue from two rat strains with widely differing sensitivities to TCDD-induced wasting syndrome: TCDD-sensitive Long–Evans rats and TCDD-resistant Han/Wistar rats, 23 h after exposure to TCDD (100 μg/kg) or corn oil vehicle. TCDD exposure caused minimal transcriptional dysregulation in the hypothalamus, with only 6 genes significantly altered in Long–Evans rats and 15 genes in Han/Wistar rats. Two of the most dysregulated genes were Cyp1a1 and Nqo1, which are induced by TCDD across a wide range of tissues and are considered sensitive markers of TCDD exposure. The minimal response of the hypothalamic transcriptome to a lethal dose of TCDD at an early time-point suggests that the hypothalamus is not the predominant site of initial events leading to hypophagia and associated wasting. TCDD may affect feeding behaviour via events upstream or downstream of the hypothalamus, and further work is required to evaluate this at the level of individual hypothalamic nuclei and subregions.
dc.language.isoeng
dc.publisherElsevier; German Toxicology Society
dc.relation.ispartofseriesToxicology
dc.subject.otherAHR
dc.subject.otherfeed restriction
dc.subject.otherhypothalamus
dc.subject.othermicroarray
dc.subject.otherTCDD
dc.titleTranscriptional profiling of rat hypothalamus response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-201509072823
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.updated2015-09-07T12:15:08Z
dc.type.coarjournal article
dc.description.reviewstatuspeerReviewed
dc.format.pagerange93-101
dc.relation.issn0300-483X
dc.relation.numberinseries3 February 2015
dc.relation.volume328
dc.type.versionpublishedVersion
dc.rights.copyright© 2014 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY license.
dc.rights.accesslevelopenAccessfi
dc.rights.urlhttp://creativecommons.org/licenses/by/4.0/
dc.relation.doi10.1016/j.tox.2014.12.016


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© 2014 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY license.
Except where otherwise noted, this item's license is described as © 2014 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY license.