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Brooks, Katie
Publications (2 of 2) Show all publications
Luijten, I. H. N., Brooks, K., Boulet, N., Shabalina, I. G., Jaiprakash, A., Carlsson, B., . . . Nedergaard, J. (2019). Glucocorticoid-Induced Obesity Develops Independently of UCP1. Cell Reports, 27(6), 1686-1698
Open this publication in new window or tab >>Glucocorticoid-Induced Obesity Develops Independently of UCP1
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2019 (English)In: Cell Reports, 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.

National Category
Biological Sciences
Identifiers
urn:nbn:se:su:diva-169257 (URN)10.1016/j.celrep.2019.04.041 (DOI)000467058500006 ()31067456 (PubMedID)
Available from: 2019-06-12 Created: 2019-06-12 Last updated: 2024-01-17Bibliographically approved
Luijten, I., Brooks, K., Boulet, N., Shabalina, I., Jaiprakash, A., Carlsson, B., . . . Nedergaard, J.Glucocorticoid-induced obesity develops independently of UCP1.
Open this publication in new window or tab >>Glucocorticoid-induced obesity develops independently of UCP1
Show others...
(English)Manuscript (preprint) (Other academic)
Abstract [en]

An excess of glucocorticoids is associated with the development of obesity, as is evident from the accumulation of visceral fat in patients suffering from Cushing’s Syndrome. Activated brown adipose tissue (BAT) reduces metabolic efficiency; correspondingly an inactivation of BAT has been proposed to cause glucocorticoid-induced obesity. Here we determine the extent to which changes in BAT function as a result of glucocorticoid treatment contribute to the simultaneous development of obesity. In mice housed at 21 °C and treated with corticosterone for 2 weeks (CORT), we unexpectedly found no change in total BAT uncoupling protein 1 (UCP1) protein levels or in non-shivering thermogenic capacity. In mice housed at thermoneutrality, a humanized condition, we did observe a reduction in total UCP1 protein levels in BAT in response to CORT, which was reflected in reduced brown adipocyte cellular and mitochondrial UCP1-dependent respiration. However, glucocorticoid-induced obesity developed to the same extent in animals housed at 21 °C and 30 °C, while total BAT UCP1 protein levels differed 100-fold between the two groups. In wild-type and UCP1 knock-out mice housed at 30 °C and treated with CORT, obesity also developed to the same extent. Thus, contrary to what has previously been suggested, our results show that the development of glucocorticoid-induced obesity is unrelated to the presence of UCP1.

Keywords
uncoupling protein 1, corticosterone, obesity, thermogenesis, energy balance, brown adipose tissue, thermoneutrality, cold exposure
National Category
Biochemistry and Molecular Biology
Research subject
Molecular Bioscience
Identifiers
urn:nbn:se:su:diva-163421 (URN)
Funder
Swedish Research Council
Available from: 2019-01-02 Created: 2019-01-02 Last updated: 2022-02-26Bibliographically approved
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