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Glucocorticoid-Induced Obesity Develops Independently of UCP1

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Glucocorticoid-Induced Obesity Develops Independently of UCP1. / Luijten, Ineke H N; Brooks, Katie; Boulet, Nathalie; Shabalina, Irina G; Jaiprakash, Ankita; Carlsson, Bo; Fischer, Alexander W; Cannon, Barbara; Nedergaard, Jan.

In: CELL REP, Vol. 27, No. 6, 07.05.2019, p. 1686-1698.e5.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Luijten, IHN, Brooks, K, Boulet, N, Shabalina, IG, Jaiprakash, A, Carlsson, B, Fischer, AW, Cannon, B & Nedergaard, J 2019, 'Glucocorticoid-Induced Obesity Develops Independently of UCP1', CELL REP, vol. 27, no. 6, pp. 1686-1698.e5. https://doi.org/10.1016/j.celrep.2019.04.041

APA

Luijten, I. H. N., Brooks, K., Boulet, N., Shabalina, I. G., Jaiprakash, A., Carlsson, B., Fischer, A. W., Cannon, B., & Nedergaard, J. (2019). Glucocorticoid-Induced Obesity Develops Independently of UCP1. CELL REP, 27(6), 1686-1698.e5. https://doi.org/10.1016/j.celrep.2019.04.041

Vancouver

Luijten IHN, Brooks K, Boulet N, Shabalina IG, Jaiprakash A, Carlsson B et al. Glucocorticoid-Induced Obesity Develops Independently of UCP1. CELL REP. 2019 May 7;27(6):1686-1698.e5. https://doi.org/10.1016/j.celrep.2019.04.041

Bibtex

@article{cb73e98d84044f6ca59be99163506f9b,
title = "Glucocorticoid-Induced Obesity Develops Independently of UCP1",
abstract = "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°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°C and 30°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°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.",
keywords = "Adipose Tissue, Brown/metabolism, Adiposity, Animals, Cell Respiration, Corticosterone/adverse effects, Down-Regulation, Feeding Behavior, Glucocorticoids/adverse effects, Mice, Mitochondria/metabolism, Obesity/etiology, Phenotype, Temperature, Transcription, Genetic, Uncoupling Protein 1/metabolism",
author = "Luijten, {Ineke H N} and Katie Brooks and Nathalie Boulet and Shabalina, {Irina G} and Ankita Jaiprakash and Bo Carlsson and Fischer, {Alexander W} and Barbara Cannon and Jan Nedergaard",
note = "Copyright {\textcopyright} 2019 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2019",
month = may,
day = "7",
doi = "10.1016/j.celrep.2019.04.041",
language = "English",
volume = "27",
pages = "1686--1698.e5",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "6",

}

RIS

TY - JOUR

T1 - Glucocorticoid-Induced Obesity Develops Independently of UCP1

AU - Luijten, Ineke H N

AU - Brooks, Katie

AU - Boulet, Nathalie

AU - Shabalina, Irina G

AU - Jaiprakash, Ankita

AU - Carlsson, Bo

AU - Fischer, Alexander W

AU - Cannon, Barbara

AU - Nedergaard, Jan

N1 - Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2019/5/7

Y1 - 2019/5/7

N2 - 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°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°C and 30°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°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.

AB - 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°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°C and 30°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°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.

KW - Adipose Tissue, Brown/metabolism

KW - Adiposity

KW - Animals

KW - Cell Respiration

KW - Corticosterone/adverse effects

KW - Down-Regulation

KW - Feeding Behavior

KW - Glucocorticoids/adverse effects

KW - Mice

KW - Mitochondria/metabolism

KW - Obesity/etiology

KW - Phenotype

KW - Temperature

KW - Transcription, Genetic

KW - Uncoupling Protein 1/metabolism

U2 - 10.1016/j.celrep.2019.04.041

DO - 10.1016/j.celrep.2019.04.041

M3 - SCORING: Journal article

C2 - 31067456

VL - 27

SP - 1686-1698.e5

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 6

ER -