Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure

Research output: Contribution to journalJournal articlepeer-review

Standard

Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure. / Nicolaisen, Trine Sand; Klein, Anders Bue; Dmytriyeva, Oksana; Lund, Jens; Ingerslev, Lars Roed; Fritzen, Andreas Mæchel; Carl, Christian Strini; Lundsgaard, Annemarie; Frost, Mikkel; Ma, Tao; Schjerling, Peter; Gerhart-Hines, Zachary; Flamant, Frederic; Gauthier, Karine; Larsen, Steen; Richter, Erik A.; Kiens, Bente; Clemmensen, Christoffer.

In: F A S E B Journal, Vol. 34, No. 11, 2020, p. 15480-15491.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Nicolaisen, TS, Klein, AB, Dmytriyeva, O, Lund, J, Ingerslev, LR, Fritzen, AM, Carl, CS, Lundsgaard, A, Frost, M, Ma, T, Schjerling, P, Gerhart-Hines, Z, Flamant, F, Gauthier, K, Larsen, S, Richter, EA, Kiens, B & Clemmensen, C 2020, 'Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure', F A S E B Journal, vol. 34, no. 11, pp. 15480-15491. https://doi.org/10.1096/fj.202001258RR

APA

Nicolaisen, T. S., Klein, A. B., Dmytriyeva, O., Lund, J., Ingerslev, L. R., Fritzen, A. M., Carl, C. S., Lundsgaard, A., Frost, M., Ma, T., Schjerling, P., Gerhart-Hines, Z., Flamant, F., Gauthier, K., Larsen, S., Richter, E. A., Kiens, B., & Clemmensen, C. (2020). Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure. F A S E B Journal, 34(11), 15480-15491. https://doi.org/10.1096/fj.202001258RR

Vancouver

Nicolaisen TS, Klein AB, Dmytriyeva O, Lund J, Ingerslev LR, Fritzen AM et al. Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure. F A S E B Journal. 2020;34(11):15480-15491. https://doi.org/10.1096/fj.202001258RR

Author

Nicolaisen, Trine Sand ; Klein, Anders Bue ; Dmytriyeva, Oksana ; Lund, Jens ; Ingerslev, Lars Roed ; Fritzen, Andreas Mæchel ; Carl, Christian Strini ; Lundsgaard, Annemarie ; Frost, Mikkel ; Ma, Tao ; Schjerling, Peter ; Gerhart-Hines, Zachary ; Flamant, Frederic ; Gauthier, Karine ; Larsen, Steen ; Richter, Erik A. ; Kiens, Bente ; Clemmensen, Christoffer. / Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure. In: F A S E B Journal. 2020 ; Vol. 34, No. 11. pp. 15480-15491.

Bibtex

@article{2c340c7f9d124172b6f450e113fce7b6,
title = "Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure",
abstract = "Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered a key site for thyroid action, the contribution of thyroid hormone receptor signaling in muscle to whole-body energy metabolism and body temperature has not been resolved. Here, we show that T3-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRα1 ) in skeletal muscle, but that T3-mediated elevation in body temperature is achieved in the absence of muscle-TRα1 . In slow-twitch soleus muscle, loss-of-function of TRα1 (TRαHSACre ) alters the fiber-type composition toward a more oxidative phenotype. The change in fiber-type composition, however, does not influence the running capacity or motivation to run. RNA-sequencing of soleus muscle from WT mice and TRαHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, providing molecular clues pertaining to the mechanistic underpinnings of TRα1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in T3-stimulated increase in whole-body energy expenditure.",
keywords = "Faculty of Science, Energy expenditure, Energy metabolism, Skeletal muscle, Thyorid hormone",
author = "Nicolaisen, {Trine Sand} and Klein, {Anders Bue} and Oksana Dmytriyeva and Jens Lund and Ingerslev, {Lars Roed} and Fritzen, {Andreas M{\ae}chel} and Carl, {Christian Strini} and Annemarie Lundsgaard and Mikkel Frost and Tao Ma and Peter Schjerling and Zachary Gerhart-Hines and Frederic Flamant and Karine Gauthier and Steen Larsen and Richter, {Erik A.} and Bente Kiens and Christoffer Clemmensen",
note = "{\textcopyright} 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.",
year = "2020",
doi = "10.1096/fj.202001258RR",
language = "English",
volume = "34",
pages = "15480--15491",
journal = "F A S E B Journal",
issn = "0892-6638",
publisher = "Federation of American Societies for Experimental Biology",
number = "11",

}

RIS

TY - JOUR

T1 - Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure

AU - Nicolaisen, Trine Sand

AU - Klein, Anders Bue

AU - Dmytriyeva, Oksana

AU - Lund, Jens

AU - Ingerslev, Lars Roed

AU - Fritzen, Andreas Mæchel

AU - Carl, Christian Strini

AU - Lundsgaard, Annemarie

AU - Frost, Mikkel

AU - Ma, Tao

AU - Schjerling, Peter

AU - Gerhart-Hines, Zachary

AU - Flamant, Frederic

AU - Gauthier, Karine

AU - Larsen, Steen

AU - Richter, Erik A.

AU - Kiens, Bente

AU - Clemmensen, Christoffer

N1 - © 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.

PY - 2020

Y1 - 2020

N2 - Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered a key site for thyroid action, the contribution of thyroid hormone receptor signaling in muscle to whole-body energy metabolism and body temperature has not been resolved. Here, we show that T3-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRα1 ) in skeletal muscle, but that T3-mediated elevation in body temperature is achieved in the absence of muscle-TRα1 . In slow-twitch soleus muscle, loss-of-function of TRα1 (TRαHSACre ) alters the fiber-type composition toward a more oxidative phenotype. The change in fiber-type composition, however, does not influence the running capacity or motivation to run. RNA-sequencing of soleus muscle from WT mice and TRαHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, providing molecular clues pertaining to the mechanistic underpinnings of TRα1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in T3-stimulated increase in whole-body energy expenditure.

AB - Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered a key site for thyroid action, the contribution of thyroid hormone receptor signaling in muscle to whole-body energy metabolism and body temperature has not been resolved. Here, we show that T3-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRα1 ) in skeletal muscle, but that T3-mediated elevation in body temperature is achieved in the absence of muscle-TRα1 . In slow-twitch soleus muscle, loss-of-function of TRα1 (TRαHSACre ) alters the fiber-type composition toward a more oxidative phenotype. The change in fiber-type composition, however, does not influence the running capacity or motivation to run. RNA-sequencing of soleus muscle from WT mice and TRαHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, providing molecular clues pertaining to the mechanistic underpinnings of TRα1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in T3-stimulated increase in whole-body energy expenditure.

KW - Faculty of Science

KW - Energy expenditure

KW - Energy metabolism

KW - Skeletal muscle

KW - Thyorid hormone

U2 - 10.1096/fj.202001258RR

DO - 10.1096/fj.202001258RR

M3 - Journal article

C2 - 32969079

VL - 34

SP - 15480

EP - 15491

JO - F A S E B Journal

JF - F A S E B Journal

SN - 0892-6638

IS - 11

ER -

ID: 249065198