Comparative Analysis of the Effects of Long-Term 3,5-diiodothyronine Treatment on the Murine Hepatic Proteome and Transcriptome Under Conditions of Normal Diet and High-Fat Diet

Lietzow, Julika; Golchert, Janine; Pietzner, Maik; Völker, Uwe; Poutanen, Matti; Ohlsson, Claes; Homuth, Georg; Köhrle, Josef

doi:10.1089/thy.2020.0160

Cited by 8 publications

(17 citation statements)

References 68 publications

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“…Similar observations were reported in skeletal muscle (Lanni et al, 2005) and brown adipose tissue (BAT) (Lombardi et al, 2015). Notably, as was demonstrated by the analysis of hepatic gene expression profile after 3,5-T2 treatment, part of the beneficial metabolic effects are mediated by canonical Type 1 T3-receptor as well as by post-translational actions of 3,5-T2, which in some way are very similar to T3's actions (Lietzow et al, 2016(Lietzow et al, , 2021. A common pathway stimulated by both T3 in myocardial infarction (De Castro et al, 2016) and 3,5-T2 (Lombardi et al, 2015) in metabolic disorders involves the peroxisome proliferator activated receptor γ co-activator 1α (PGC-1α).…”

Section: Discussionsupporting

confidence: 75%

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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Section: Discussionsupporting

confidence: 75%

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

Louzada

Padrón

Neto

et al. 2021

Experimental Physiology

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“…In addition, T2 may preserve liver mitochondrial integrity by inducing protective repair mechanisms against mtDNA oxidative stress (46). Lietzow J. et al have recently confirmed the beneficial hepatic fat reduction by T2 and induction of fatty acid oxidation in mice fed a HFD (39). Moreover, we have recently shown that, in white adipose tissue, T2 induces adipocyte browning (44), affects adipocyte morphology (already measurable after 2 weeks and persistent at 4 weeks of treatment) and tissue vascularization (47).…”

Section: Introductionsupporting

confidence: 61%

“…In the last decades many laboratories have demonstrated that T2 exhibits interesting favorable effects in different metabolically active tissues such as liver (34)(35)(36)(37)(38)(39), skeletal muscle (40,41), heart (42), and adipose tissues (43,44). In male wistar rats housed at thermoneutrality and fed on a high fat diet, simultaneous T2 administration reduces hepatic fat accumulation and hyperlipidemia (34), and induces a protein profile favoring a shift toward type 2 skeletal muscle fibers (40).…”

Section: Introductionmentioning

confidence: 99%

3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet

et al. 2021

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3,5-diiodo-thyronine (T2), an endogenous metabolite of thyroid hormones, exerts beneficial metabolic effects. When administered to overweight rats receiving a high fat diet (HFD), it significantly reduces body fat accumulation, which is a risk factor for the development of an inflammatory state and of related metabolic diseases. In the present study, we focused our attention on T2 actions aimed at improving the adverse effects of long-lasting HFD such as the adipocyte inflammatory response. For this purpose, three groups of rats were used throughout: i) receiving a standard diet for 14 weeks; ii) receiving a HFD for 14 weeks, and iii) receiving a HFD for 14 weeks with a simultaneous daily injection of T2 for the last 4 weeks. The results showed that T2 administration ameliorated the expression profiles of pro- and anti-inflammatory cytokines, reduced macrophage infiltration in white adipose tissue, influenced their polarization and reduced lymphocytes recruitment. Moreover, T2 improved the expression of hypoxia markers, all altered in HFD rats, and reduced angiogenesis by decreasing the pro-angiogenic miR126 expression. Additionally, T2 reduced the oxidative damage of DNA, known to be associated to the inflammatory status. This study demonstrates that T2 is able to counteract some adverse effects caused by a long-lasting HFD and to produce beneficial effects on inflammation. Irisin and SIRT1 pathway may represent a mechanism underlying the above described effects.

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“…In rat skeletal muscle, T2 has resulted to stimulate mitochondrial uncoupling [126,130]. Interestingly, metabolic and lipid-lowering effects of T2 have also been shown in mice [131][132][133].…”

Section: Nongenomic Regulation Of Mitochondrial Respiratory Chain By ...mentioning

confidence: 97%

Bioenergetic Aspects of Mitochondrial Actions of Thyroid Hormones

Cioffi

Giacco

Goglia

et al. 2022

Cells

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Much is known, but there is also much more to discover, about the actions that thyroid hormones (TH) exert on metabolism. Indeed, despite the fact that thyroid hormones are recognized as one of the most important regulators of metabolic rate, much remains to be clarified on which mechanisms control/regulate these actions. Given their actions on energy metabolism and that mitochondria are the main cellular site where metabolic transformations take place, these organelles have been the subject of extensive investigations. In relatively recent times, new knowledge concerning both thyroid hormones (such as the mechanisms of action, the existence of metabolically active TH derivatives) and the mechanisms of energy transduction such as (among others) dynamics, respiratory chain organization in supercomplexes and cristes organization, have opened new pathways of investigation in the field of the control of energy metabolism and of the mechanisms of action of TH at cellular level. In this review, we highlight the knowledge and approaches about the complex relationship between TH, including some of their derivatives, and the mitochondrial respiratory chain.

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Comparative Analysis of the Effects of Long-Term 3,5-diiodothyronine Treatment on the Murine Hepatic Proteome and Transcriptome Under Conditions of Normal Diet and High-Fat Diet

Cited by 8 publications

References 68 publications

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

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

3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet

Bioenergetic Aspects of Mitochondrial Actions of Thyroid Hormones

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