Treatment of hypothyroid rats with T2 (3,5-di-iodo-<scp>l</scp>-thyronine) rapidly stimulates respiration in subsequently isolated mitochondria

O'Reilly, Ian; Murphy, Michael P.

doi:10.1042/bst020059s

Cited by 8 publications

(3 citation statements)

References 3 publications

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“…We found that hypothyroid rats survived cold for 3–4 days, but when injected with 3,5‐T2 their cold tolerance was improved, with an effect on both the specific and total oxidase activity of the analysed organs, and the animals survived, like those treated with T3, for at least the duration of the treatment. However, the action of 3,5‐T2 does not affect the tissue trophism, and we, on the basis of previous studies (O'Reilly & Murphy 1992b, Goglia et al. 1994a,b), raised the possibility that the effects exerted by 3,5‐T2 may be mediated by its direct interaction with mitochondria.…”

Section: Thyroid Hormones and Coldmentioning

confidence: 67%

Thyroid hormones as molecular determinants of thermogenesis

Silvestri

Schiavo

Lombardi

et al. 2005

Acta Physiologica Scandinavica

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Thyroid hormones (TH) are major modulators of energy metabolism and thermogenesis. It is generally believed that 3,5,3'-triiodo-l-thyronine (T3) is the only active form of TH, and that most of its effects are mediated by nuclear T3 receptors, which chiefly affect the transcription of target genes. Some of these genes encode for the proteins involved in energy metabolism. However, a growing volume of evidence now indicates that other iodothyronines may be biologically active. Several mechanisms have been proposed to explain the calorigenic effect of TH, but none has received universal acceptance. Cold acclimation/exposure and altered nutritional status are physiological conditions in which a modulation of energy expenditure is particularly important. TH seem to be deeply involved in this modulation, and this article will review some aspects of their possible influence in these conditions.

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Section: Thyroid Hormones and Coldmentioning

confidence: 67%

Thyroid hormones as molecular determinants of thermogenesis

Silvestri

Schiavo

Lombardi

et al. 2005

Acta Physiologica Scandinavica

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“…3,5‐T 2 was initially shown to rapidly stimulate respiratory rate in isolated rat liver mitochondria (O'Reilly & Murphy ) and to enhance oxygen consumption in rat liver (Horst et al . ), but not glucose uptake in human mononuclear blood cells (Kvetny ).…”

Section: Diiodothyroninesmentioning

confidence: 99%

Emerging role of thyroid hormone metabolites

et al. 2016

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Thyroid hormones (THs) are essential for the regulation of development and metabolism in key organs. THs produce biological effects both by directly affecting gene expression through the interaction with nuclear receptors (genomic effects) and by activating protein kinases and/or ion channels (short-term effects). Such activations can be either direct, in the case of ion channels, or mediated by membrane or cytoplasmic receptors. Short-term-activated signalling pathways often play a role in the regulation of genomic effects. Several TH intermediate metabolites, which were previously considered without biological activity, have now been associated with a broad range of actions, mostly attributable to short-term effects. Here, we give an overview of the physiological roles and mechanisms of action of THs, focusing on the emerging position that TH metabolites are acquiring as important regulators of physiology and metabolism.

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“…3,5-Diiodothyronine (3,5-T2) is a product of T3 outer ring deiodination that increases oxygen consumption in perfused rat liver (Horst et al, 1989), blood mononuclear cells (Kvetny, 1992) and rat liver mitochondria (Lanni et al, 1993;O'Reilly & Murphy, 1992), resembling the metabolic effects of T3 and T4. Remarkably, 3,5-T2 has been shown to prevent liver steatosis in rats fed a high-fat diet.…”

Section: Introductionmentioning

confidence: 99%

3,5‐Diiodothyronine protects against cardiac ischaemia–reperfusion injury in male rats

Louzada

Padrón

Neto

et al. 2021

Experimental Physiology

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The use of 3,5,3′-triiodothyronine (T3) and thyroxine (T4) to treat metabolic diseases has been hindered by potential adverse effects on liver, lipid metabolism and cardiac electrical properties. It is recognized that 3,5-diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models and ameliorates insulin resistance, suggesting 3,5-T2 as a potential therapeutic tool.However, a comprehensive assessment of cardiac electrical and contractile properties has not been made so far. Three-month-old Wistar rats were daily administered vehicle, 3,5-T2 or 3,5-T2+T4 and no signs of atrial or ventricular arrhythmia were detected in non-anaesthetized rats during 90 days. Cardiac function was preserved as heart rate, left ventricle diameter and shortening fraction in 3,5-T2-treated rats compared to vehicle and 3,5-T2+T4 groups. Power spectral analysis indicated an amelioration of the heart rate variability only in 3,5-T2-treated rats. An increased baroreflex sensitivity at rest was observed in both 3,5-T2-treated groups. Finally, 3,5-T2 Langendorff-perfused hearts presented a significant recovery of left ventricular function and remarkably smaller infarction area after ischaemia-reperfusion injury. In conclusion, chronic 3,5-T2 administration ameliorates tonic cardiac autonomic control

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Treatment of hypothyroid rats with T2 (3,5-di-iodo-l-thyronine) rapidly stimulates respiration in subsequently isolated mitochondria

Abstract: Administration of T3 to hypothyroid rats increases the respiration rate of the subsequently isolated mitochondria [1,2]. This effect, and a number of other rapid effects of T3, occur

Cited by 8 publications

References 3 publications

Thyroid hormones as molecular determinants of thermogenesis

Thyroid hormones as molecular determinants of thermogenesis

Emerging role of thyroid hormone metabolites

3,5‐Diiodothyronine protects against cardiac ischaemia–reperfusion injury in male rats

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