scholarly journals Looking for the Mechanism of Action of Thyroid Hormone

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Jamshed R. Tata

The mechanisms of action of thyroid hormone (TH), characterized by multiple physiological activities, proposed over the last 80 years are a reflection of the progression of our knowledge about eukaryotic signalling processes. The cumulative knowledge gained raises the question as to what is so special about the action of this hormone. The discovery in the 1980s that TH receptors belong to the family of nuclear transcription factors that regulate the expression of hormonal target genes was an important milestone. TH receptors are highly organized within the chromatin structure, which itself is modified by several chromosomal and nonchromosomal factors, in the presence and absence of the hormone. Recently, some investigators have suggested that TH acts via both genomic and nongenomic mechanisms and introduced the concept of networking within cellular complexes. While one cannot as yet precisely describe the mechanism of thyroid hormone action, I will attempt here to point out the present thinking and future directions to achieve this goal in the light of the historical background.

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrice Chatonnet ◽  
Frédéric Picou ◽  
Teddy Fauquier ◽  
Frédéric Flamant

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.


2014 ◽  
Vol 122 (03) ◽  
Author(s):  
H Rakov ◽  
K Engels ◽  
D Zwanziger ◽  
M Renders ◽  
K Brix ◽  
...  

2011 ◽  
Vol 74 (3) ◽  
pp. 346-353 ◽  
Author(s):  
Sebastián Susperreguy ◽  
Liliana Muñoz ◽  
Natalia Y. Tkalenko ◽  
Ivan D. Mascanfroni ◽  
Vanina A. Alamino ◽  
...  

1975 ◽  
Vol 292 (20) ◽  
pp. 1063-1068 ◽  
Author(s):  
Howard L. Bleich ◽  
Emily S. Boro ◽  
Jack H. Oppenheimer

Thyroid ◽  
2021 ◽  
Author(s):  
Marek Strączkowski ◽  
Agnieszka Nikołajuk ◽  
Magdalena Stefanowicz ◽  
Natalia Matulewicz ◽  
José Manuel Fernández-Real ◽  
...  

1995 ◽  
Vol 132 (4) ◽  
pp. 413-418 ◽  
Author(s):  
MJ Müller ◽  
CA Reynard ◽  
AG Burger ◽  
G Toffolo ◽  
C Cobelli ◽  
...  

Müller MJ, Reynard CA, Burger AG, Toffolo G, Cobelli C, Ferrannini E. Kinetic analysis of thyroid hormone action on glucose metabolism in man. Eur J Endocrinol 1995;132:413–18. ISSN 0804–4643 Thyroid hormone action on insulin's effect on glucose kinetics was investigated with the use of a physiological three compartment model. In six healthy volunteers before and after 14 days of thyroxine treatment (300 μg/day), a bolus of [3-H3]glucose was injected and the time course of plasma radioactivity was followed closely for 150 min. Then a hyperinsulinemic (1 mU · min−1 · kg−1) and euglycemic clamp was started, and euglycemia was maintained for another 250 min. A second bolus of the tracer was then given at 240 min, and the plasma radioactivity was followed for 160 min. Insulin stimulated basal plasma glucose clearance fourfold (p < 0.001) and completely suppressed basal hepatic glucose production (p < 0.001). Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Thyroxine treatment increased plasma triiodothyronine by about 20% (0.1 > p > 0.05) but did not affect basal glucose turnover, insulin-stimulated plasma glucose clearance or the insulin-induced suppression of endogenous glucose output. However, thyroxine treatment blunted the insulin-induced increases in total distribution volume and the slowly exchanging pool of glucose (p = NS vs the basal state). We conclude that minor changes in plasma triiodothyronine (such as occur during overfeeding) do not interfere with the ability of insulin to stimulate the rate of disappearance of glucose or suppress endogenous glucose release; however, our data suggest that they induce finer changes in glucose kinetics, possibly reflecting acceleration or intracellular glucose degradation. Manfred J Müller, Institut für Humanernährung und Lebensmittelkunde, Christian-Albrechts-Universität zu Kiel, Düsternbrooker Weg 17, D-24105 Kiel, Germany


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