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Metabolism and Diseases Related to Thyroid Function

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 5164

Special Issue Editors


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Guest Editor
Department of Internal Medicine, Division of Endocrinology and Metabolism, Gunma University Graduate School of Medicine, 3-39-15, Showa, Maebashi 371-8511, Japan
Interests: thyroid; pituitary; TSH; thyroid hormone; thyroid hormone receptor; cancer; diabetes mellitus

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Guest Editor
Division of Endocrinology and Metabolism, Department of Internal Medicine, Gunma University Graduate School of Medicine, Maebashi, Japan
Interests: thyroid; endocrinology; diabetes medicine

Special Issue Information

Dear Colleagues,

Thyroid hormones play a crucial role in the metabolism of glucose, lipids, and proteins—intricate biochemical processes within our bodies. These hormones, primarily thyroxine (T4) and triiodothyronine (T3), are secreted by the thyroid gland and are stimulated by pituitary thyroid-stimulating hormone (TSH). The feedback loop system associated with thyroid hormone production and release significantly impacts the rate at which our cells utilize energy. Their influence spans across nearly every tissue and organ, including the heart, brain, muscles, and digestive system.

This Special Issue aims to bring together cutting-edge research and insights into the mechanisms underlying thyroid hormone action, metabolism regulation, and therapeutic interventions. Submissions from researchers and clinicians in the field of endocrinology, biochemistry, and related disciplines are encouraged.

We welcome the submission of original research articles that explore the intricate relationship between thyroid hormone function and metabolism, as well as their implications in diseases such as hypothyroidism, hyperthyroidism, and thyroid cancer. Pure clinical or model studies will not be suitable for this journal. However, clinical or pure model submissions with biomolecular experiments are welcomed.

Dr. Eijiro Yamada
Dr. Shunichi Matsumoto
Guest Editors

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Keywords

  • thyroid function
  • metabolism
  • diabetes mellitus
  • dyslipidemia
  • obesity
  • cancer

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Published Papers (3 papers)

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Research

20 pages, 4833 KiB  
Article
The Downregulation of the Liver Lipid Metabolism Induced by Hypothyroidism in Male Mice: Metabolic Flexibility Favors Compensatory Mechanisms in White Adipose Tissue
by Lamis Chamas, Isabelle Seugnet, Odessa Tanvé, Valérie Enderlin and Marie-Stéphanie Clerget-Froidevaux
Int. J. Mol. Sci. 2024, 25(19), 10792; https://doi.org/10.3390/ijms251910792 - 8 Oct 2024
Viewed by 1070
Abstract
In mammals, the maintenance of energy homeostasis relies on complex mechanisms requiring tight synchronization between peripheral organs and the brain. Thyroid hormones (THs), through their pleiotropic actions, play a central role in these regulations. Hypothyroidism, which is characterized by low circulating TH levels, [...] Read more.
In mammals, the maintenance of energy homeostasis relies on complex mechanisms requiring tight synchronization between peripheral organs and the brain. Thyroid hormones (THs), through their pleiotropic actions, play a central role in these regulations. Hypothyroidism, which is characterized by low circulating TH levels, slows down the metabolism, which leads to a reduction in energy expenditure as well as in lipid and glucose metabolism. The objective of this study was to evaluate whether the metabolic deregulations induced by hypothyroidism could be avoided through regulatory mechanisms involved in metabolic flexibility. To this end, the response to induced hypothyroidism was compared in males from two mouse strains, the wild-derived WSB/EiJ mouse strain characterized by a diet-induced obesity (DIO) resistance due to its high metabolic flexibility phenotype and C57BL/6J mice, which are prone to DIO. The results show that propylthiouracil (PTU)-induced hypothyroidism led to metabolic deregulations, particularly a reduction in hepatic lipid synthesis in both strains. Furthermore, in contrast to the C57BL/6J mice, the WSB/EiJ mice were resistant to the metabolic dysregulations induced by hypothyroidism, mainly through enhanced lipid metabolism in their adipose tissue. Indeed, WSB/EiJ mice compensated for the decrease in hepatic lipid synthesis by mobilizing lipid reserves from white adipose tissue. Gene expression analysis revealed that hypothyroidism stimulated the hypothalamic orexigenic circuit in both strains, but there was unchanged melanocortin 4 receptor (Mc4r) and leptin receptor (LepR) expression in the hypothyroid WSB/EiJ mice strain, which reflects their adaptability to maintain their body weight, in contrast to C57BL/6J mice. Thus, this study showed that WSB/EiJ male mice displayed a resistance to the metabolic dysregulations induced by hypothyroidism through compensatory mechanisms. This highlights the importance of metabolic flexibility in the ability to adapt to disturbed circulating TH levels. Full article
(This article belongs to the Special Issue Metabolism and Diseases Related to Thyroid Function)
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18 pages, 5535 KiB  
Article
Transcriptomic Analysis Reveals That Excessive Thyroid Hormone Signaling Impairs Phototransduction and Mitochondrial Bioenergetics and Induces Cellular Stress in Mouse Cone Photoreceptors
by Hongwei Ma, David Stanford, Willard M. Freeman and Xi-Qin Ding
Int. J. Mol. Sci. 2024, 25(13), 7435; https://doi.org/10.3390/ijms25137435 - 6 Jul 2024
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Abstract
Thyroid hormone (TH) plays an essential role in cell proliferation, differentiation, and metabolism. Experimental and clinical studies have shown a potential association between TH signaling and retinal degeneration. The suppression of TH signaling protects cone photoreceptors in mouse models of retinal degeneration, whereas [...] Read more.
Thyroid hormone (TH) plays an essential role in cell proliferation, differentiation, and metabolism. Experimental and clinical studies have shown a potential association between TH signaling and retinal degeneration. The suppression of TH signaling protects cone photoreceptors in mouse models of retinal degeneration, whereas excessive TH signaling induces cone degeneration, manifested as reduced light response and a loss of cones. This work investigates the genes/transcriptomic alterations that might be involved in TH-induced cone degeneration in mice using single-cell RNA sequencing (scRNAseq) analysis. One-month-old C57BL/6 mice received triiodothyronine (T3, 20 µg/mL in drinking water) for 4 weeks as a model of hyperthyroidism/excessive TH signaling. At the end of the experiments, retinal cells were dissociated, and cell viability was analyzed before being subjected to scRNAseq. The resulting data were analyzed using the Seurat package and visualized using the Loupe browser. Among 155,866 single cells, we identified 14 cell clusters, representing various retinal cell types, with rod and cone clusters comprising 76% and 4.1% of the total cell population, respectively. Cone cluster transcriptomes demonstrated the most alterations after the T3 treatment, with 450 differentially expressed genes (DEGs), accounting for 38.5% of the total DEGs. Statistically significant changes in the expression of genes in the cone cluster revealed that phototransduction and oxidative phosphorylation were impaired after the T3 treatment, along with mitochondrial dysfunction. A pathway analysis also showed the activation of the sensory neuronal/photoreceptor stress pathways after the T3 treatment. Specifically, the eukaryotic initiation factor-2 signaling pathway and the cAMP response element-binding protein signaling pathway were upregulated. Thus, excessive TH signaling substantially affects cones at the transcriptomic level. The findings from this work provide an insight into how excessive TH signaling induces cone degeneration. Full article
(This article belongs to the Special Issue Metabolism and Diseases Related to Thyroid Function)
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11 pages, 2418 KiB  
Article
Role of Thyroid Hormone in Dynamic Variation of gdf6a Gene during Metamorphosis of Paralichthys olivaceus
by Yaxin Shi, Junqiang Qiu, Xike Li, Yue Lin, Wenjuan Li, Jilun Hou and Yuanshuai Fu
Int. J. Mol. Sci. 2024, 25(1), 23; https://doi.org/10.3390/ijms25010023 - 19 Dec 2023
Cited by 1 | Viewed by 1220
Abstract
The Japanese flounder (Paralichthys olivaceus) is a marine fish that undergoes a dramatic postembryonic metamorphosis, with the right eye shifting to the left and its lifestyle transitioning from planktonic to benthic. As the light environment of the habitat changes from bright [...] Read more.
The Japanese flounder (Paralichthys olivaceus) is a marine fish that undergoes a dramatic postembryonic metamorphosis, with the right eye shifting to the left and its lifestyle transitioning from planktonic to benthic. As the light environment of the habitat changes from bright to dim, its photoreceptor system also undergoes adaptive change. Growth differentiation factor 6a (Gdf6a) is a member of the BMP family, which plays a key role in regulating the dorsal–ventral pattern of the retina and photoreceptor fate, and the differentiation of different photoreceptors is also modulated by a thyroid hormone (TH) binding its receptor (TR). However, the relationship between gdf6a and TH and its role in the regulation of photoreceptors during flounder metamorphosis is still poorly understood. In this study, bioinformatics analysis showed that Gdf6a had a conserved TGFB structural domain and clusters with fishes. The expression analysis showed that the expression of gdf6a was highest in the eye tissue of adult flounder and tended to increase and then decrease during metamorphosis, reaching its highest levels at the peak of metamorphosis. Moreover, the expression of gdf6a increased in the early stages of metamorphosis after exogenous TH treatment, while it was inhibited after exogenous thiourea (a TH inhibitor, TU) treatment. To further investigate the targeting role of TH and gdf6a in the metamorphosis of flounder, the results of the Dual-Luciferase revealed that triiodothyronine (T3) may regulate the expression of gdf6a through TRβ. In conclusion, we speculate that TH influences the development of cone photoreceptors during the metamorphosis of the flounder by regulating the expression of gdf6a. Full article
(This article belongs to the Special Issue Metabolism and Diseases Related to Thyroid Function)
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