Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-l-thyronine
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Tri-iodothyronine (T3) and thyroxine (T4) as well as 3,5-di-iodothyronine (T2) stimulated O2 consumption by isolated perfused livers from hypothyroid rats at a concentration as low as 1 pM by about 30% within 90 min. Application of T2 resulted in a faster stimulation than with application of T3 or T4. Inhibition of iodothyronine monodeiodinase by propylthiouracil, thereby blocking the degradation of T4 to T3 and of T3 to T2, demonstrated that only T2 is the active hormone for the rapid stimulation of hepatic O2 consumption: T3 and T4 lost all of their stimulative activity, whereas T2 was as potent as in the absence of propylthiouracil. Perfusion experiments with thyroid-hormone analogues confirmed the specificity of the T2 effect. The nucleus is unlikely to contribute to the rapid T2 effect, as can be deduced from perfusion experiments with cycloheximide and lack of induction of malic enzyme by T2. In conclusion, a new scheme of regulation of mitochondrial activity is proposed: T2 acts rapidly and directly via a mitochondrial pathway, whereas T3 exerts its long-term action indirectly by induction of specific enzymes.
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3,5-T2 increases the rate of oxygen consumption in perfused rat liver, blood mononuclear cells, and rat liver mitochondria.
“Compound 3,5-T2 by itself increases the rate of oxygen consumption in perfused rat liver (Horst et al. 1989), blood mononuclear cells (Kvetny 1992), and rat liver mitochondria (Lanni et al. 1992, 1993, O'Reilly & Murphy 1992)”
From Administration of 3,5-diiodothyronine (3,5-T2) causes central hypothyroidism and stimulates thyroid-sensitive tissues (2014) · cites this paper as Horst et al. 1989
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- Authors
- Horst, C., Rokos, H., & Seitz, H. J.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- Henning Berlin G.m.b.H., Research Laboratory, D-1000 Berlin 42, Germany
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 1989-08-01
- Volume
- 261
- Issue
- 3
- Pages
- 945-950
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC1138920
- OpenAlex
- W1766142764
- Cited by
- 119
- References
- 0
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2022: 4 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 7 · 2017: 3 · 2016: 2 · 2015: 4 · 2014: 6 · 2013: 4
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- 3,5-diiodothyronine, hepatic oxygen consumption, triiodothyronine, thyroxine, propylthiouracil, isolated perfused liver, thyroid hormone action, mitochondrial activity, malic enzyme, cycloheximide
- MeSH terms
- Animals, Diiodothyronines, Hypothyroidism, Male, Mitochondria, Liver, Oxygen Consumption, Rats, Inbred Strains, Stimulation, Chemical, Thyronines, Thyroxine, Triiodothyronine, Reverse, Rats
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