Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption
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Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption. / Johann, Kornelia; Cremer, Anna Lena; Fischer, Alexander W; Heine, Markus; Pensado, Eva Rial; Resch, Julia; Nock, Sebastian; Virtue, Samuel; Harder, Lisbeth; Oelkrug, Rebecca; Astiz, Mariana; Brabant, Georg; Warner, Amy; Vidal-Puig, Antonio; Oster, Henrik; Boelen, Anita; López, Miguel; Heeren, Joerg; Dalley, Jeffrey W; Backes, Heiko; Mittag, Jens.
In: CELL REP, Vol. 27, No. 11, 11.06.2019, p. 3385-3400.e3.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption
AU - Johann, Kornelia
AU - Cremer, Anna Lena
AU - Fischer, Alexander W
AU - Heine, Markus
AU - Pensado, Eva Rial
AU - Resch, Julia
AU - Nock, Sebastian
AU - Virtue, Samuel
AU - Harder, Lisbeth
AU - Oelkrug, Rebecca
AU - Astiz, Mariana
AU - Brabant, Georg
AU - Warner, Amy
AU - Vidal-Puig, Antonio
AU - Oster, Henrik
AU - Boelen, Anita
AU - López, Miguel
AU - Heeren, Joerg
AU - Dalley, Jeffrey W
AU - Backes, Heiko
AU - Mittag, Jens
N1 - Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
PY - 2019/6/11
Y1 - 2019/6/11
N2 - Regulation of body temperature critically depends on thyroid hormone (TH). Recent studies revealed that TH induces browning of white adipose tissue, possibly contributing to the observed hyperthermia in hyperthyroid patients and potentially providing metabolic benefits. Here, we show that browning by TH requires TH-receptor β and occurs independently of the sympathetic nervous system. The beige fat, however, lacks sufficient adrenergic stimulation and is not metabolically activated despite high levels of uncoupling protein 1 (UCP1). Studies at different environmental temperatures reveal that TH instead causes hyperthermia by actions in skeletal muscle combined with a central body temperature set-point elevation. Consequently, the metabolic and thermogenic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents.
AB - Regulation of body temperature critically depends on thyroid hormone (TH). Recent studies revealed that TH induces browning of white adipose tissue, possibly contributing to the observed hyperthermia in hyperthyroid patients and potentially providing metabolic benefits. Here, we show that browning by TH requires TH-receptor β and occurs independently of the sympathetic nervous system. The beige fat, however, lacks sufficient adrenergic stimulation and is not metabolically activated despite high levels of uncoupling protein 1 (UCP1). Studies at different environmental temperatures reveal that TH instead causes hyperthermia by actions in skeletal muscle combined with a central body temperature set-point elevation. Consequently, the metabolic and thermogenic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents.
KW - Adipose Tissue, Beige/metabolism
KW - Adipose Tissue, Brown/metabolism
KW - Adipose Tissue, White/metabolism
KW - Animals
KW - Glucose/metabolism
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Muscle, Skeletal/metabolism
KW - Receptors, Adrenergic, beta-3/metabolism
KW - Thermogenesis
KW - Thyroid Hormones/metabolism
KW - Uncoupling Protein 1/genetics
U2 - 10.1016/j.celrep.2019.05.054
DO - 10.1016/j.celrep.2019.05.054
M3 - SCORING: Journal article
C2 - 31189119
VL - 27
SP - 3385-3400.e3
JO - CELL REP
JF - CELL REP
SN - 2211-1247
IS - 11
ER -