scholarly journals Thyroid Hormone Action and Energy Expenditure

2019 ◽  
Vol 3 (7) ◽  
pp. 1345-1356 ◽  
Author(s):  
Sahzene Yavuz ◽  
Silvia Salgado Nunez del Prado ◽  
Francesco S Celi
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure ◽  
Hormone Receptors ◽  
Hormone Replacement ◽  
Critical Role ◽  
Hormone Action ◽  
Energy Status ◽  
Thyroid Hormone Action ◽  
Thyroid Hormone Replacement Therapy ◽  
Hormonal Signal

Abstract Energy metabolism is one of the most recognized targets of thyroid hormone action, which indeed plays a critical role in modulating energy expenditure in all of its components. This is because thyroid hormone receptors are ubiquitous, and thyroid hormones interact and influence most metabolic pathways in virtually all systems throughout the entire life of the organism. The pleiotropic actions of thyroid hormone are the results of interaction between the local availability of T3 and the signal transduction machinery, which confer in physiologic conditions time and tissue specificity of the hormonal signal despite negligible variations in circulating levels. Historically, the measurement of energy expenditure has been used as the gold standard for the clinical assessment of the hormonal action until the advent of the immunoassays for TSH and thyroid hormone, which have since been used as proxy for measurement of thyroid hormone action. Although the clinical correlates between thyroid hormone action and energy expenditure in cases of extreme dysfunction (florid hyperthyroidism or hypothyroidism) are well recognized, there is still controversy on the effects of moderate, subclinical thyroid dysfunction on energy expenditure and, ultimately, on body weight trajectory. Moreover, little information is available on the effects of thyroid hormone replacement therapy on energy expenditure. This mini review is aimed to define the clinical relevance of thyroid hormone action in normal physiology and functional disorders, as well the effects of thyroid hormone therapy on energy expenditure and the effects of changes in energy status on the thyroid hormone axis.

scholarly journals Combination Treatment with T4 and T3: Toward Personalized Replacement Therapy in Hypothyroidism?

2012 ◽  
Vol 97 (7) ◽  
pp. 2256-2271 ◽  
Author(s):  
Bernadette Biondi ◽  
Leonard Wartofsky
Keyword(s):  
Quality Of Life ◽  
Thyroid Hormone ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Hormone Action ◽  
Thyroid Hormone Replacement ◽  
Thyroid Hormone Action ◽  
Thyroid Hormone Replacement Therapy ◽  
Hypothyroid Patients

Abstract Context: Levothyroxine therapy is the traditional lifelong replacement therapy for hypothyroid patients. Over the last several years, new evidence has led clinicians to evaluate the option of combined T3 and T4 treatment to improve the quality of life, cognition, and peripheral parameters of thyroid hormone action in hypothyroidism. The aim of this review is to assess the physiological basis and the results of current studies on this topic. Evidence Acquisition: We searched Medline for reports published with the following search terms: hypothyroidism, levothyroxine, triiodothyronine, thyroid, guidelines, treatment, deiodinases, clinical symptoms, quality of life, cognition, mood, depression, body weight, heart rate, cholesterol, bone markers, SHBG, and patient preference for combined therapy. The search was restricted to reports published in English since 1970, but some reports published before 1970 were also incorporated. We supplemented the search with records from personal files and references of relevant articles and textbooks. Parameters analyzed included the rationale for combination treatment, the type of patients to be selected, the optimal T4/T3 ratio, and the potential benefits of this therapy on symptoms of hypothyroidism, quality of life, mood, cognition, and peripheral parameters of thyroid hormone action. Evidence Synthesis: The outcome of our analysis suggests that it may be time to consider a personalized regimen of thyroid hormone replacement therapy in hypothyroid patients. Conclusions: Further prospective randomized controlled studies are needed to clarify this important issue. Innovative formulations of the thyroid hormones will be required to mimic a more perfect thyroid hormone replacement therapy than is currently available.

scholarly journals Reduced pituitary size in subjects with mutations in the THRB gene and thyroid hormone resistance

2021 ◽  
Author(s):  
Marcus Heldmann ◽  
Krishna Chatterjee ◽  
Carla Moran ◽  
Berenike Rogge ◽  
Julia Steinhardt ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Pituitary Gland ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Magnetic Resonance Images ◽  
Healthy Controls ◽  
Hormone Action ◽  
Resistance To Thyroid Hormone ◽  
Thyroid Hormone Action ◽  
Thyroid Hormone Receptor Β

Background: Thyroid hormone action is mediated by two forms of thyroid hormone receptors (α,β) with differential tissue distribution. Thyroid hormone receptor β (TRβ) mutations lead to resistance to thyroid hormone action in tissues predominantly expressing the β form of the receptor (pituitary, liver). This study seeks to identify effects of mutant TRβ on pituitary size. Methods: High-resolution 3D T1-weighted magnetic resonance images were acquired in 19 patients with RTHβ in comparison to 19 healthy matched controls. Volumetric measurements of the pituitary gland were performed independently and blinded by four different raters (two neuroradiologists, one neurologist, one neuroscientist). Results: Patients with mutant TRβ (Resistance to Thyroid Hormone β,RΤΗβ) showed elevated fT3/4 levels with normal TSH levels, whereas healthy controls showed normal thyroid hormone levels. Imaging revealed smaller pituitary size in RTHβ patients in comparison to healthy controls (F(1,35)=7.05, p=0.012, partial η2 =0.17). Conclusion: RTHβ subjects have impaired sensitivity to thyroid hormones, along with decreased size of the pituitary gland.

Molecular mechanisms of sex-dependent thyroid hormone action on target tissues

2014 ◽  
Vol 122 (03) ◽  
Author(s):  
H Rakov ◽  
K Engels ◽  
D Zwanziger ◽  
M Renders ◽  
K Brix ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Molecular Mechanisms ◽  
Hormone Action ◽  
Thyroid Hormone Action

Thyroid hormones regulate phosphate homoeostasis through transcriptional control of the renal type IIa sodium-dependent phosphate co-transporter (Npt2a) gene

2010 ◽  
Vol 427 (1) ◽  
pp. 161-169 ◽  
Author(s):  
Mariko Ishiguro ◽  
Hironori Yamamoto ◽  
Masashi Masuda ◽  
Mina Kozai ◽  
Yuichiro Takei ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Molecular Mechanisms ◽  
Hormone Receptors ◽  
Critical Role ◽  
Serum Phosphate ◽  
Luciferase Assay ◽  
Mobility Shift ◽  
Intron 1 ◽  
Sodium Dependent

The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. It has been demonstrated previously that renal Npt2a protein and its mRNA expression are both up-regulated by the thyroid hormone T3 (3,3′,5-tri-iodothyronine) in rats. However, it has never been established whether the induction was mediated by a direct effect of thyroid hormones on the Npt2a promoter. To address the role of Npt2a in T3-dependent regulation of phosphate homoeostasis and to identify the molecular mechanisms by which thyroid hormones modulate Npt2a gene expression, mice were rendered pharmacologically hypo- and hyper-thyroid. Hypothyroid mice showed low levels of serum phosphate and a marked decrease in renal Npt2a protein abundance. Importantly, we also showed that Npt2a-deficient mice had impaired serum phosphate responsiveness to T3 compared with wild-type mice. Promoter analysis with a luciferase assay revealed that the transcriptional activity of a reporter gene containing the Npt2a promoter and intron 1 was dependent upon TRs (thyroid hormone receptors) and specifically increased by T3 in renal cells. Deletion analysis and EMSAs (electrophoretic mobility-shift assays) determined that there were unique TREs (thyroid-hormone-responsive elements) within intron 1 of the Npt2a gene. These results suggest that Npt2a plays a critical role as a T3-target gene, to control phosphate homoeostasis, and that T3 transcriptionally activates the Npt2a gene via TRs in a renal cell-specific manner.

Growth hormone treatment in children with idiopathic short stature: correlation of growth response with peripheral thyroid hormone action

2011 ◽  
Vol 74 (3) ◽  
pp. 346-353 ◽  
Author(s):  
Sebastián Susperreguy ◽  
Liliana Muñoz ◽  
Natalia Y. Tkalenko ◽  
Ivan D. Mascanfroni ◽  
Vanina A. Alamino ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormone ◽  
Short Stature ◽  
Growth Response ◽  
Growth Hormone Treatment ◽  
Hormone Treatment ◽  
Idiopathic Short Stature ◽  
Hormone Action ◽  
Thyroid Hormone Action

scholarly journals Thyroid Hormone Action in Cerebellum and Cerebral Cortex Development

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrice Chatonnet ◽  
Frédéric Picou ◽  
Teddy Fauquier ◽  
Frédéric Flamant
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Glial Cell ◽  
Nuclear Receptors ◽  
Target Genes ◽  
Cell Types ◽  
Hormone Action ◽  
Cerebral Cortex Development ◽  
Thyroid Hormone Action

Thyroid hormones (TH, including the prohormone thyroxine (T4) and its active deiodinated derivative 3,,5-triiodo-L-thyronine (T3)) are important regulators of vertebrates neurodevelopment. Specific transporters and deiodinases are required to ensure T3 access to the developing brain. T3 activates a number of differentiation processes in neuronal and glial cell types by binding to nuclear receptors, acting directly on transcription. Only few T3 target genes are currently known. Deeper investigations are urgently needed, considering that some chemicals present in food are believed to interfere with T3 signaling with putative neurotoxic consequences.

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