Depressed Thermogenesis but Competent Brown Adipose Tissue Recruitment in Mice Devoid of All Hormone-Binding Thyroid Hormone Receptors
Abstract
We have examined the metabolic role of hormone-binding nuclear thyroid hormone receptors (TRs). Mice devoid of all hormone-binding TRs [TR alpha 1(-/-)beta(-/-) (TR-ablated mice)] had slightly decreased body temperature and much decreased basal metabolic rate, were still able to markedly increase metabolic rate in the cold, but were cold intolerant due to inadequate total heat production at low temperatures. A standard norepinephrine test showed that adrenergically induced thermogenesis could not be activated normally in the TR-ablated mice. This was not due to inadequate recruitment of brown adipose tissue, nor to the absence, decreased recruitment or dysfunction of the uncoupling protein-1. However, isolated brown fat cells were 10-fold desensitized, explaining the lack of response to standard adrenergic stimuli; cell culture experiments demonstrated that this desensitization was not an innate effect. Thus, the cold intolerance was probably not due to inadequate sympathetically induced nonshivering thermogenesis. Additionally, the results indicated that no metabolic effects of thyroid hormones could become manifest in the absence of nuclear TRs, that ligand-bound TRs were needed for euthermia and eumetabolism, but that TRs per se were not required for brown adipose tissue recruitment and uncoupling protein-1 gene expression.
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Type 2 iodothyronine deiodinase plays a critical role in regulating the amount of active thyroid hormone, triiodothyronine, in brown fat, thereby modulating adaptive thermogenesis.
“Type 2 iodothyronine deiodinase plays a critical role in regulating the amount of active thyroid hormone, triiodothyronine, in brown fat, thereby modulating adaptive thermogenesis 64,65.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [64]
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- Authors
- Golozoubova, V., Gullberg, H., Matthias, A., Cannon, B., Vennström, B., & Nedergaard, J.
- Affiliations
- Stockholm University (SE)
- Karolinska Institutet (SE)
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2004-02
- Volume
- 18
- Issue
- 2
- Pages
- 384-401
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W2124055916
- Cited by
- 155
- References
- 91
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 4 · 2022: 6 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 2 · 2017: 9 · 2016: 6 · 2015: 9 · 2014: 18 · 2013: 12 · 2012: 8
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- thyroid hormone receptor, thermogenesis, cold sensitivity, UCP1, receptor desensitization, basal metabolic rate, body temperature, thyroid hormone signaling
- MeSH terms
- Uncoupling Protein 1, Adrenergic alpha-Agonists, Animals, Adipose Tissue, Brown, Carrier Proteins, Cells, Cultured, Cold Temperature, Female, Gene Expression Regulation, Ion Channels, Male, Membrane Proteins, Mice, Mutant Strains, Norepinephrine, Receptors, Thyroid Hormone, Thermogenesis, Mitochondrial Proteins, Thyroid Hormone Receptors alpha, Thyroid Hormone Receptors beta, Mice
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