Thyroid Hormone Effects on Mitochondrial Energetics
Abstract
Thyroid hormones are the major endocrine regulators of metabolic rate, and their hypermetabolic effects are widely recognized. The cellular mechanisms underlying these metabolic effects have been the subject of much research. Thyroid hormone status has a profound impact on mitochondria, the organelles responsible for the majority of cellular adenosine triphosphate (ATP) production. However, mechanisms are not well understood. We review the effects of thyroid hormones on mitochondrial energetics and principally oxidative phosphorylation. Genomic and nongenomic mechanisms have been studied. Through the former, thyroid hormones stimulate mitochondriogenesis and thereby augment cellular oxidative capacity. Thyroid hormones induce substantial modifications in mitochondrial inner membrane protein and lipid compositions. Results are consistent with the idea that thyroid hormones activate the uncoupling of oxidative phosphorylation through various mechanisms involving inner membrane proteins and lipids. Increased uncoupling appears to be responsible for some of the hypermetabolic effects of thyroid hormones. ATP synthesis and turnover reactions are also affected. There appear to be complex relationships between mitochondrial proton leak mechanisms, reactive oxygen species production, and thyroid status. As the majority of studies have focused on the effects of thyroid status on rat liver preparations, there is still a need to address fundamental questions regarding thyroid hormone effects in other tissues and species.
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Both T3 and T2 are known to regulate mitochondrial activity in skeletal muscle.
“Of note, both T3 and T2 are known to regulate mitochondrial activity in skeletal muscle [45, 46].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [45]
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Atzmon, G., Barzilai, N., Surks, M. I., & Gabriely, I. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0808 · Cited by 145 · see citing works
Johannsen, D. L., Galgani, J. E., Johannsen, N. M., Zhang, Z., Covington, J. D., & Ravussin, E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0040837 · Cited by 57 · see citing works
- Authors
- Harper, M.-E., & Seifert, E. L.
- Affiliations
- University of Ottawa (CA)
- ORCID
- Harper, Mary-Ellen
- Venue
- Thyroid
- Publisher
- SAGE Publications
- Published
- 2008-02
- Volume
- 18
- Issue
- 2
- Pages
- 145-156
- ISSN
- 1050-7256 (ISSN-L)
- 1557-9077
- OpenAlex
- W1965505826
- Cited by
- 194
- References
- 99
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 12 · 2023: 12 · 2022: 18 · 2021: 10 · 2020: 19 · 2019: 4 · 2018: 7 · 2017: 8 · 2016: 12 · 2015: 10 · 2014: 7 · 2013: 7 · 2012: 11
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Thyroid (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- thyroid hormones, mitochondrial bioenergetics, oxidative phosphorylation, hypermetabolism, uncoupling, mitochondrial biogenesis, mitochondrial inner membrane proteins, mitochondrial lipids, proton leak, reactive oxygen species, ATP production, genomic mechanisms, liver mitochondria
- MeSH terms
- Adenosine Triphosphate, Animals, Energy Metabolism, Humans, Membrane Lipids, Mitochondria, Oxidative Phosphorylation, Thyroid Hormones, Reactive Oxygen Species, Mitochondrial Membranes, Mice, Rats
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