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Glucocorticoid-Induced Obesity Develops Independently of UCP1
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
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Number of Authors: 92019 (English)In: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 27, no 6, p. 1686-1698Article in journal (Refereed) Published
Abstract [en]

An excess of glucocorticoids leads to the development of obesity in both mice and humans, but the mechanism for this is unknown. Here, we determine the extent to which decreased BAT thermogenic capacity (as a result of glucocorticoid treatment) contributes to the development of obesity. Contrary to previous suggestions, we show that only in mice housed at thermoneutrality (30 degrees C) does corticosterone treatment reduce total BAT UCP1 protein. This reduction is reflected in reduced brown adipocyte cellular and mitochondrial UCP1-dependent respiration. However, glucocorticoid-induced obesity develops to the same extent in animals housed at 21 degrees C and 30 degrees C, whereas total BAT UCP1 protein levels differ 100-fold between the two groups. In corticosterone-treated wild-type and UCP1 knockout mice housed at 30 degrees C, obesity also develops to the same extent. Thus, our results demonstrate that the development of glucocorticoid-induced obesity is not caused by a decreased UCP1-dependent thermogenic capacity.

Place, publisher, year, edition, pages
2019. Vol. 27, no 6, p. 1686-1698
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Biological Sciences
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URN: urn:nbn:se:su:diva-169257DOI: 10.1016/j.celrep.2019.04.041ISI: 000467058500006PubMedID: 31067456OAI: oai:DiVA.org:su-169257DiVA, id: diva2:1323502
Available from: 2019-06-12 Created: 2019-06-12 Last updated: 2019-06-12Bibliographically approved

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Luijten, Ineke H. N.Brooks, KatieBoulet, NathalieShabalina, Irina G.Fischer, Alexander W.Cannon, BarbaraNedergaard, Jan
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