Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption.

Autor:	Johann K; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Cremer AL; Multimodal Imaging of Brain Metabolism, Max Planck Institute of Metabolism Research, 50931 Cologne, Germany., Fischer AW; Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Heine M; Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Pensado ER; NeurObesity Group, Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela 15782, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela 15782, Spain., Resch J; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Nock S; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Virtue S; University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UK., Harder L; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Oelkrug R; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Astiz M; Institute of Neurobiology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Brabant G; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Warner A; University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UK., Vidal-Puig A; University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UK., Oster H; Institute of Neurobiology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany., Boelen A; Laboratory of Endocrinology, Amsterdam University Medical Centers, 1105 Amsterdam, the Netherlands., López M; NeurObesity Group, Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela 15782, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela 15782, Spain., Heeren J; Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Dalley JW; Department of Psychology, University of Cambridge, Cambridge CB2 3EB, UK; Department of Psychiatry, University of Cambridge, Cambridge CB2 2QQ, UK., Backes H; Multimodal Imaging of Brain Metabolism, Max Planck Institute of Metabolism Research, 50931 Cologne, Germany., Mittag J; Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany. Electronic address: jens.mittag@uni-luebeck.de.
Jazyk:	angličtina
Zdroj:	Cell reports [Cell Rep] 2019 Jun 11; Vol. 27 (11), pp. 3385-3400.e3.
DOI:	10.1016/j.celrep.2019.05.054
Abstrakt:	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. (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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