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dc.contributor.authorFitzpatrick, Susan F
dc.contributor.authorGojkovic, Milos
dc.contributor.authorMacias, David
dc.contributor.authorTegnebratt, Tetyana
dc.contributor.authorLu, Li
dc.contributor.authorSamén, Erik
dc.contributor.authorRundqvist, Helene
dc.contributor.authorJohnson, Randall
dc.date.accessioned2019-01-17T00:30:29Z
dc.date.available2019-01-17T00:30:29Z
dc.date.issued2018
dc.identifier.issn1664-042X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/288093
dc.description.abstractThe in vivo response to lipopolysaccharide (LPS) occurs rapidly and has profound physiological and metabolic effects. The hypoxia inducible (HIF) transcription factor is an intrinsic and essential part of inflammation, and is induced by LPS. To determine the importance of the HIF response in regulating metabolism following an LPS response, glucose uptake was quantified in a time dependent manner in mice lacking HIF-1α in myeloid cells. We found that deletion of HIF-1α has an acute protective effect on LPS-induced hypoglycemia. Furthermore, reduced glucose uptake was observed in the heart and brown fat, in a time dependent manner, following loss of HIF-1α. To determine the physiological significance of these findings, cardiovascular, body temperature, and blood pressure changes were subsequently quantified in real time using radiotelemetry measurements. These studies reveal the temporal aspects of HIF-1α as a regulator of the metabolic response to acute LPS-induced inflammation.
dc.description.sponsorshipFunded by a PRF award from the Wellcome Trust and by the Swedish Research Council (Vetenskapsrådet), Swedish Cancer Fund (Cancerfonden) and Swedish Children's Cancer Fund (Barncancerfonden).
dc.format.mediumElectronic-eCollection
dc.languageeng
dc.publisherFrontiers Media SA
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleGlycolytic Response to Inflammation Over Time: Role of Myeloid HIF-1alpha.
dc.typeArticle
prism.publicationDate2018
prism.publicationNameFront Physiol
prism.startingPage1624
prism.volume9
dc.identifier.doi10.17863/CAM.35408
dcterms.dateAccepted2018-10-26
rioxxterms.versionofrecord10.3389/fphys.2018.01624
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
rioxxterms.licenseref.startdate2018-01
dc.contributor.orcidJohnson, Randall [0000-0002-4084-6639]
dc.identifier.eissn1664-042X
rioxxterms.typeJournal Article/Review
pubs.funder-project-idWellcome Trust (092738/Z/10/Z)
pubs.funder-project-idNational Cancer Institute (R01CA153983)
pubs.funder-project-idEuropean Commission (331756)
pubs.funder-project-idWellcome Trust (214283/Z/18/Z)
cam.issuedOnline2018-11-22


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International