scholarly journals Developmentally defined regulation of thyroid hormone metabolism by glucocorticoids in the rat

2005 ◽  
Vol 185 (2) ◽  
pp. 327-336 ◽  
Author(s):  
S Van der Geyten ◽  
V M Darras
Keyword(s):  
Thyroid Hormone ◽  
Direct Consequence ◽  
Type I ◽  
Hormone Metabolism ◽  
Hormone Levels ◽  
Thyroid Hormone Metabolism ◽  
Rat Pups ◽  
Short Period ◽  
Thyroid Hormone Levels

Glucocorticoids are known regulators of thyroid function in vertebrates. In birds they have clear tissue-specific and age-dependent effects on thyroid hormone metabolism. In mammals, however, few studies exist addressing these aspects using an in vivo model system. We therefore set out to examine the acute effects of a single dose of dexamethasone (DEX) on plasma 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) levels, as well as on the activity of the different deiodinases in liver, kidney and brain in the developing rat. In 20-day-old fetuses (E20), glucocorticoids had no effects on circulating thyroid hormone levels despite their clear effects on hepatic and renal deiodinases, thereby indicating that under these conditions circulating thyroid hormone levels are more dependent on thyroidal secretion than on peripheral deiodination. In contrast, in 5-day-old rat pups, DEX did not seem to have any effects on hepatic and renal T3 production (via the type I deiodinase), whereas type III deiodinase (D3) activity in both these tissues increased significantly. These observations therefore suggested that the DEX-induced increase in circulating T3 levels is a direct consequence of the increase in plasma T4 levels. In 12-day-old pups (P12), however, the main effect of glucocorticoids on circulating levels was by increasing inner ring deiodination T3 through induction of D3 in both liver and kidney. Finally, in the brain, glucocorticoids stimulated thyroid hormone activity only during a short period of time (between E20 and P12) that largely overlaps with the transient window in time during which brain development is thyroid hormone sensitive. This was in contrast to the E20 and P12 brain, where the glucocorticoid-induced changes in type II deiodinase and D3 seemed to favor a status quo in local T3 availability.

The role of selenium in thyroid hormone metabolism

1991 ◽  
Vol 69 (11) ◽  
pp. 1648-1652 ◽  
Author(s):  
John R. Arthur
Keyword(s):  
Thyroid Hormone ◽  
Iodine Deficiency ◽  
Selenium Deficiency ◽  
Major Influence ◽  
Type I ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Iodothyronine Deiodinases ◽  
Clinical Changes

In animals, decreases in selenium-containing glutathione peroxidase activity and the resultant impairment of peroxide metabolism can account for many, but not all of the biochemical and clinical changes caused by selenium deficiency. Recently, however, type I iodothyronine 5′-deiodinase has also been shown to be a selenium-containing enzyme. This explains the impairment of thyroid hormone metabolism caused by selenium deficiency in animals with a normal vitamin E status. Since iodothyronine 5′-deiodinases are essential for the production of the active thyroid hormone 3,5,3′-triiodothyronine, some of the consequences of selenium deficiency may result from thyroid changes rather than inability to metabolise peroxides. In particular, the impaired thyroid hormone metabolism may be responsible for decreased growth and resistance to cold stress in selenium-deficient animals. A further consequence of the role of selenium in thyroid hormone metabolism is the exacerbation of some of the thyroid changes in iodine deficiency by a concurrent selenium deficiency. Selenium status may therefore have a major influence on the outcome of iodine deficiency in both human and animal populations.Key words: selenium, thyroid hormones, iodothyronine deiodinases, iodine, nutritional disorders.

scholarly journals Tissue Deiodinase Activity during Prolonged Critical Illness: Effects of Exogenous Thyrotropin-Releasing Hormone and Its Combination with Growth Hormone-Releasing Peptide-2

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5604-5611 ◽  
Author(s):  
Yves Debaveye ◽  
Björn Ellger ◽  
Liese Mebis ◽  
Erik Van Herck ◽  
Willy Coopmans ◽  
...  
Keyword(s):  
Critical Illness ◽  
Thyroid Hormone ◽  
In Vivo Model ◽  
Joint Control ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Tsh Secretion ◽  
Underlying Mechanisms ◽  
To Receive

Prolonged critical illness is characterized by reduced pulsatile TSH secretion, causing reduced thyroid hormone release and profound changes in thyroid hormone metabolism, resulting in low circulating T3 and elevated rT3 levels. To further unravel the underlying mechanisms, we investigated the effects of exogenous TRH and GH-releasing peptide-2 (GHRP-2) in an in vivo model of prolonged critical illness. Burn-injured, parenterally fed rabbits were randomized to receive 4-d treatment with saline, 60 μg/kg·h GHRP-2, 60 μg/kg·h TRH, or 60 μg/kg·h TRH plus 60 μg/kg·h GHRP-2 started on d 4 of the illness (n = 8/group). The activities of the deiodinase 1 (D1), D2, and D3 in snap-frozen liver, kidney, and muscle as well as their impact on circulating thyroid hormone levels were studied. Compared with healthy controls, hepatic D1 activity in the saline-treated, ill animals was significantly down-regulated (P = 0.02), and D3 activity tended to be up-regulated (P = 0.06). Infusion of TRH and TRH plus GHRP-2 restored the catalytic activity of D1 (P = 0.02) and increased T3 levels back within physiological range (P = 0.008). D3 activity was normalized by all three interventions, but only addition of GHRP-2 to TRH prevented the rise in rT3 seen with TRH alone (P = 0.02). Liver D1 and D3 activity were correlated (respectively, positively and negatively) with the changes in circulating T3 (r = 0.84 and r = −0.65) and the T3/rT3 ratio (r = 0.71 and r = −0.60). We conclude that D1 activity during critical illness is suppressed and related to the alterations within the thyrotropic axis, whereas D3 activity tends to be increased and under the joint control of the somatotropic and thyrotropic axes.

scholarly journals Effects of concomitant selenium and vitamin E administration on thyroid hormone metabolism in broilers

2018 ◽  
Vol 68 (3) ◽  
pp. 355
Author(s):  
A. C. PAPPAS ◽  
B. M. KOTSAMPASI ◽  
K. KALAMARAS ◽  
K. FEGEROS ◽  
G. ZERVAS ◽  
...  
Keyword(s):  
Vitamin E ◽  
Thyroid Hormone ◽  
Control Diet ◽  
Dietary Treatment ◽  
Tocopheryl Acetate ◽  
Type I ◽  
Hormone Metabolism ◽  
Iodothyronine Deiodinase ◽  
Thyroid Hormone Metabolism ◽  
Diet Control

A total of 400, as hatched, broilers were used to investigate the effect of selenium (Se) and vitamin E supplementation on thyroid hormones metabolism. There were 5 replicates of 4 dietary treatments namely: control (C), a soybean meal maize basal diet with adequate Se and vitamin E (0.3 mg Se per kg diet and 80 mg vitamin E per kg diet), control diet with Se added (Se+, with an additional 1 mg of Se per kg of diet), control diet with vitamin E added (E+, with an additional 350 mg of vitamin E per kg of diet) and Se+E+ (with additional 1 mg of Se and 350 mg of vitamin E per kg of diet). Diets were isonitrogenous and isocaloric. Zinc L-selenomethionine complex was used to increase Se content and dl-α-tocopheryl acetate to increase vitamin E content. The experiment lasted 42 days. Plasma Se concentration increased in Se+ groups, while whole blood glutathione peroxidase (GPx) activity increased in Se+, E+ and Se+E+ groups compared to control. Hepatic type I iodothyronine deiodinase (ID-I) and thyroid hormone concentrations were unaffected by any dietary treatment. It is concluded that supplementation with Se or vitamin Ε alone or in combination above animal’s requirements does not affect thyroid hormone metabolism and liver ID-I activity under the conditions examined.

scholarly journals Iodothyronine deiodinases and the control of plasma and tissue thyroid hormone levels in hyperthyroid tilapia (Oreochromis niloticus)

2005 ◽  
Vol 184 (3) ◽  
pp. 467-479 ◽  
Author(s):  
S Van der Geyten ◽  
N Byamungu ◽  
G E Reyns ◽  
E R Kühn ◽  
V M Darras
Keyword(s):  
Thyroid Hormone ◽  
Oreochromis Niloticus ◽  
Degradation Mechanism ◽  
Current Data ◽  
Type I ◽  
Iodothyronine Deiodinase ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

Thyroid status is one of the most potent regulators of peripheral thyroid hormone metabolism in vertebrates. Despite this, the few papers that have been published concerning the role of thyroid hormones in the regulation of thyroid function in fish often offer conflicting data. We therefore set out to investigate the effects of tetraiodothyronine (thyroxine) (T4) or tri-iodothyronine (T3) supplementation (48 p.p.m.) via the food on plasma and tissue thyroid hormone levels as well as iodothyronine deiodinase (D) activities in the Nile tilapia (Oreochromis niloticus). T4 supplementation did not induce a hyperthyroid state and subsequently had no effects on the thyroid hormone parameters measured, with the liver as the sole notable exception. In T4-fed tilapias, the hepatic T4 levels increased substantially, and this was accompanied by an increase in in vitro type I deiodinase (D1) activity. Although the lack of effect of T4 supplementation could be partially explained by an inefficient uptake of T4 from the gut, our current data suggest that also the increased conversion of T4 into reverse (r)T3 by the D1 present in the liver plays an important role in this respect. In addition, T3 supplementation increased plasma T3 and decreased plasma T4 concentrations. T3 levels were also increased in the liver, brain, kidney, gill and white muscle, but without affecting local T4 concentrations. However, this increase in T3 availability remained without effect on D1 activity in liver and kidney. This observation, together with the 6-n-propylthiouracyl (PTU) insensitivity of the D1 enzyme in fish, sets the D1 in teleost fish clearly apart from its mammalian and avian counterparts. The changes in hepatic deiodinases confirm the role of the liver as an important T3-regulating tissue. However, the very short plasma half-life of exogenously administered T3 implies the existence of an efficient T3 clearing/degradation mechanism other than deiodination.

scholarly journals Thyroid Hormone Receptor α Modulates Lipopolysaccharide-Induced Changes in Peripheral Thyroid Hormone Metabolism

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1959-1969 ◽  
Author(s):  
Joan Kwakkel ◽  
Olivier Chassande ◽  
Hermina C. van Beeren ◽  
Eric Fliers ◽  
Wilmar M. Wiersinga ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Acute Illness ◽  
Sublethal Dose ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Serum T3 ◽  
Thyroid Hormone Receptor Α

Acute inflammation is characterized by low serum T3 and T4 levels accompanied by changes in liver type 1 deiodinase (D1), liver D3, muscle D2, and muscle D3 expression. It is unknown at present whether thyroid hormone receptor α (TRα) plays a role in altered peripheral thyroid hormone metabolism during acute illness in vivo. We induced acute illness in TRα-deficient (TRα0/0) mice by administration of a sublethal dose of LPS. Compared with wild-type, TRα0/0 mice have lower basal serum T4 and lower liver D1 activity and muscle D3 mRNA expression, whereas liver D3 activity is higher. These changes are gender specific. The inflammatory response to LPS was similar in WT and TRα0/0 mice. The decrease in serum thyroid hormones and liver D1 was attenuated in TRα0/0 mice, whereas the LPS induced fall in liver D3 mRNA was more pronounced in TRα0/0 mice. Muscle D2 mRNA increased similarly in both strains, whereas muscle D3 mRNA decreased less pronounced in TRα0/0 mice. We conclude that alterations in peripheral thyroid hormone metabolism induced by LPS administration are partly regulated via TRα.

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