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Thyroid Hormone Protects from Fasting-Induced Skeletal Muscle Atrophy by Promoting Metabolic Adaptation.

Authors
  • Ucci, Sarassunta1
  • Renzini, Alessandra2
  • Russi, Valentina1
  • Mangialardo, Claudia1
  • Cammarata, Ilenia1
  • Cavioli, Giorgia2
  • Santaguida, Maria Giulia3
  • Virili, Camilla3
  • Centanni, Marco3
  • Adamo, Sergio2
  • Moresi, Viviana2
  • Verga-Falzacappa, Cecilia1, 3
  • 1 Pasteur Institute, 00161 Rome, Italy. , (Italy)
  • 2 DAHFMO Unit of Histology and Medical Embryology, Interuniversity Institute of Myology, Sapienza University of Rome, 00161 Rome, Italy. , (Italy)
  • 3 Department of Medico-Surgical Sciences and Biotechnologies Sapienza University of Rome, 04100 Latina, Italy. , (Italy)
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Nov 15, 2019
Volume
20
Issue
22
Identifiers
DOI: 10.3390/ijms20225754
PMID: 31731814
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Thyroid hormones regulate a wide range of cellular responses, via non-genomic and genomic actions, depending on cell-specific thyroid hormone transporters, co-repressors, or co-activators. Skeletal muscle has been identified as a direct target of thyroid hormone T3, where it regulates stem cell proliferation and differentiation, as well as myofiber metabolism. However, the effects of T3 in muscle-wasting conditions have not been yet addressed. Being T3 primarily responsible for the regulation of metabolism, we challenged mice with fasting and found that T3 counteracted starvation-induced muscle atrophy. Interestingly, T3 did not prevent the activation of the main catabolic pathways, i.e., the ubiquitin-proteasome or the autophagy-lysosomal systems, nor did it stimulate de novo muscle synthesis in starved muscles. Transcriptome analyses revealed that T3 mainly affected the metabolic processes in starved muscle. Further analyses of myofiber metabolism revealed that T3 prevented the starvation-mediated metabolic shift, thus preserving skeletal muscle mass. Our study elucidated new T3 functions in regulating skeletal muscle homeostasis and metabolism in pathological conditions, opening to new potential therapeutic approaches for the treatment of skeletal muscle atrophy.

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