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dc.contributor.authorVirtue, Samuel
dc.contributor.authorPetkevicius, Kasparas
dc.contributor.authorMoreno-Navarrete, José Maria
dc.contributor.authorJenkins, Benjamin
dc.contributor.authorHart, Daniel
dc.contributor.authorDale, Martin
dc.contributor.authorKoulman, Albert
dc.contributor.authorFernández-Real, José Manuel
dc.contributor.authorVidal-Puig, Antonio
dc.date.accessioned2018-11-05T10:25:44Z
dc.date.available2018-11-05T10:25:44Z
dc.date.issued2018-08-21
dc.identifier.issn2211-1247
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/284598
dc.description.abstractOne understudied function of white adipose tissue (AT) is its role in postprandial lipid buffering. In this study, we demonstrate that mice lacking the adipose tissue-specific transcription factor peroxisome proliferator-activated receptor γ2 (PPARγ2) exhibit a defect in their rate of adipose tissue lipid storage. Impaired adipose tissue storage rate reduces metabolic flexibility, without compromising fasted glucose tolerance or insulin sensitivity, even following prolonged high-fat feeding. However, acutely overfeeding PPARγ2-KO mice caused a 10-fold increase in insulin levels compared with controls. Although impaired adipose tissue storage rate did not result in insulin resistance in young mice, 1-year-old PPARγ2-KO mice developed skeletal muscle insulin resistance. Our data indicate that failed adipose tissue storage may occur prior to defects in glucose handling and that overfeeding protocols may uncover genes controlling adipose tissue storage rate, as opposed to capacity, and act as a diagnostic test for early-stage human metabolic disease.
dc.format.mediumPrint
dc.languageeng
dc.publisherElsevier BV
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAdipose Tissue
dc.subjectAnimals
dc.subjectHumans
dc.subjectMice
dc.subjectLipids
dc.subjectPPAR gamma
dc.subjectCarbohydrate Metabolism
dc.titlePeroxisome Proliferator-Activated Receptor γ2 Controls the Rate of Adipose Tissue Lipid Storage and Determines Metabolic Flexibility.
dc.typeArticle
prism.endingPage2012.e7
prism.issueIdentifier8
prism.publicationDate2018
prism.publicationNameCell Rep
prism.startingPage2005
prism.volume24
dc.identifier.doi10.17863/CAM.31972
dcterms.dateAccepted2018-07-18
rioxxterms.versionofrecord10.1016/j.celrep.2018.07.063
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-08
dc.contributor.orcidKoulman, Albert [0000-0001-9998-051X]
dc.contributor.orcidVidal-Puig, Antonio [0000-0003-4220-9577]
dc.identifier.eissn2211-1247
rioxxterms.typeJournal Article/Review
pubs.funder-project-idWellcome Trust (100574/Z/12/Z)
pubs.funder-project-idBritish Heart Foundation (None)
pubs.funder-project-idMedical Research Council (MC_UU_12012/2)
pubs.funder-project-idMedical Research Council (MC_UU_12012/5)
pubs.funder-project-idMedical Research Council (G0600717)
pubs.funder-project-idMedical Research Council (G0802051)
pubs.funder-project-idMedical Research Council (MC_G0802535)
pubs.funder-project-idMedical Research Council (G0400192)
pubs.funder-project-idMRC (MC_UU_00014/2)
pubs.funder-project-idMRC (MC_UU_00014/5)
pubs.funder-project-idBritish Heart Foundation (RG/18/7/33636)


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