Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption
Summary: 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 b...
Main Authors: | , , , , , , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Elsevier
2019-06-01
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Series: | Cell Reports |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124719306837 |
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author | Kornelia Johann Anna Lena Cremer Alexander W. Fischer Markus Heine Eva Rial Pensado Julia Resch Sebastian Nock Samuel Virtue Lisbeth Harder Rebecca Oelkrug Mariana Astiz Georg Brabant Amy Warner Antonio Vidal-Puig Henrik Oster Anita Boelen Miguel López Joerg Heeren Jeffrey W. Dalley Heiko Backes Jens Mittag |
author_facet | Kornelia Johann Anna Lena Cremer Alexander W. Fischer Markus Heine Eva Rial Pensado Julia Resch Sebastian Nock Samuel Virtue Lisbeth Harder Rebecca Oelkrug Mariana Astiz Georg Brabant Amy Warner Antonio Vidal-Puig Henrik Oster Anita Boelen Miguel López Joerg Heeren Jeffrey W. Dalley Heiko Backes Jens Mittag |
author_sort | Kornelia Johann |
collection | DOAJ |
description | Summary: 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. : Thyroid hormone induces browning of white fat, but it is unclear whether this contributes to thermogenesis. Here, Johann et al. show that thyroid-hormone-induced beige fat is metabolically inactive due to lack of central stimulation and that the metabolic and thermogenic effects of the hormone are independent of UCP1. Keywords: brown adipose tissue, beige adipose tissue, uncoupling protein 1, thyroid hormone receptor, body temperature, norepinephrine, sympathetic nervous system, metabolism, beta3-adrenergic receptor, pyrexia, hyperthermia, glucose tolerance |
first_indexed | 2024-12-11T07:54:29Z |
format | Article |
id | doaj.art-a8468d419f564aed8e19c14e15682794 |
institution | Directory Open Access Journal |
issn | 2211-1247 |
language | English |
last_indexed | 2024-12-11T07:54:29Z |
publishDate | 2019-06-01 |
publisher | Elsevier |
record_format | Article |
series | Cell Reports |
spelling | doaj.art-a8468d419f564aed8e19c14e156827942022-12-22T01:15:16ZengElsevierCell Reports2211-12472019-06-01271133853400.e3Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose ConsumptionKornelia Johann0Anna Lena Cremer1Alexander W. Fischer2Markus Heine3Eva Rial Pensado4Julia Resch5Sebastian Nock6Samuel Virtue7Lisbeth Harder8Rebecca Oelkrug9Mariana Astiz10Georg Brabant11Amy Warner12Antonio Vidal-Puig13Henrik Oster14Anita Boelen15Miguel López16Joerg Heeren17Jeffrey W. Dalley18Heiko Backes19Jens Mittag20Internal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyMultimodal Imaging of Brain Metabolism, Max Planck Institute of Metabolism Research, 50931 Cologne, GermanyDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyNeurObesity 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, SpainInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UKInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyInstitute of Neurobiology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UKUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 0QQ, UKInstitute of Neurobiology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, GermanyLaboratory of Endocrinology, Amsterdam University Medical Centers, 1105 Amsterdam, the NetherlandsNeurObesity 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, SpainDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Psychology, University of Cambridge, Cambridge CB2 3EB, UK; Department of Psychiatry, University of Cambridge, Cambridge CB2 2QQ, UKMultimodal Imaging of Brain Metabolism, Max Planck Institute of Metabolism Research, 50931 Cologne, GermanyInternal Medicine I, Molecular Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, 23562 Lübeck, Germany; Corresponding authorSummary: 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. : Thyroid hormone induces browning of white fat, but it is unclear whether this contributes to thermogenesis. Here, Johann et al. show that thyroid-hormone-induced beige fat is metabolically inactive due to lack of central stimulation and that the metabolic and thermogenic effects of the hormone are independent of UCP1. Keywords: brown adipose tissue, beige adipose tissue, uncoupling protein 1, thyroid hormone receptor, body temperature, norepinephrine, sympathetic nervous system, metabolism, beta3-adrenergic receptor, pyrexia, hyperthermia, glucose tolerancehttp://www.sciencedirect.com/science/article/pii/S2211124719306837 |
spellingShingle | Kornelia Johann Anna Lena Cremer Alexander W. Fischer Markus Heine Eva Rial Pensado Julia Resch Sebastian Nock Samuel Virtue Lisbeth Harder Rebecca Oelkrug Mariana Astiz Georg Brabant Amy Warner Antonio Vidal-Puig Henrik Oster Anita Boelen Miguel López Joerg Heeren Jeffrey W. Dalley Heiko Backes Jens Mittag Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption Cell Reports |
title | Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption |
title_full | Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption |
title_fullStr | Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption |
title_full_unstemmed | Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption |
title_short | Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption |
title_sort | thyroid hormone induced browning of white adipose tissue does not contribute to thermogenesis and glucose consumption |
url | http://www.sciencedirect.com/science/article/pii/S2211124719306837 |
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