Control of Peripheral Thyroid Hormone Levels by Activating and Inactivating Deiodinases

Darras, Veerle; Mol, K.; Geyten, Serge Van der; Kühn, Eduard

doi:10.1111/j.1749-6632.1998.tb10736.x

Cited by 30 publications

(11 citation statements)

References 18 publications

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“…We do not know how much of this excess T 4 passed into the brain (Robbins and Lakshmanan, 1992). Nor do we know whether other potential buffering mechanisms such as levels of deiodinase and endogenous binding proteins might have attenuated the impact of the T 4 dosage employed (McNabb and Hughes, 1983;McNabb and Freeman, 1990;Darras et al, 1998;Rudas et al, 1993). Nevertheless, our quantitative and spatial analyses suggest that T 4 increased cell death selectively in brain regions that normally exhibit cell turnover.…”

Section: Discussionmentioning

confidence: 97%

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Tekumalla¹,

Tontonoz²,

Hesla³

et al. 2002

J. Neurobiol.

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Widespread telencephalic neuronal replacement occurs throughout life in birds. We explored the potential relationship between thyroxine (T4) and cell turnover in the adult male zebra finch. We found that many cells in the zebra finch brain, including long-projection neurons in the high vocal center (HVC), stained positively with an antibody to thyroid hormone receptors (TR). Labeling was generally weak in the ventricular zone (VZ) that gives rise to new neurons but some proliferative VZ cells and/or their progeny, identified by [3H]-thymidine labeling, co-labeled with anti-TR antibody. Acute T4 treatment dramatically increased the number of pyknotic and TUNEL-positive cells in HVC and other telencephalic regions. In contrast, degenerating cells were never observed in the archistriatum or sub-telencephalic regions, suggesting that excess T4 augments cell death selectively in regions that show naturally occurring neuronal turnover. VZ mitotic activity was not altered shortly after acute T4 treatment at a dosage that stimulated cell death, although [3H]-labeling intensity per cell was slightly reduced. Moreover, the incorporation rates for neurons formed shortly before or after acute hormone treatment were no different from control values. Chronic T4 treatment resulted in a reduction in the total number of HVC neurons. Thus, hyperthyroidism augmented neuronal death, which was not compensated for by neuronal replacement. Collectively, these results indicate that excess T4 affects adult neuronal turnover in birds, and raises the possibility that thyroxine plays an important role in the postnatal development of the avian brain and vocal behavior.

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Section: Discussionmentioning

confidence: 97%

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Tekumalla¹,

Tontonoz²,

Hesla³

et al. 2002

J. Neurobiol.

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“…In the chicken, however, starvation increased hepatic 5-deiodination (degradation of T3 to 3,3'-diiodothyronine) while hepatic 5'-deiodination (production of T3 from T4) was not affected (Darras et al, 1995(Darras et al, , 1998Van der Geyten et al, 1999). In the rat, it was reported that starvation decreased hepatic 5'-deiodination (O'Mara et al, 1993;Darras et al, 1995) and increased hepatic 5-deiodination (Darras et al, 1995(Darras et al, , 1998.…”

Section: Dependent Variablementioning

confidence: 99%

Effects of Starvation and Refeeding on Gonadotropin and Thyrotropin Subunit mRNAs in Male Japanese Quail

Kobayashi

Cockrem²,

Ishii

2002

Zoological Science

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“…reverse T 3 , di, and monoiodothyronine, as well as totally unsubstituted thyronine. T 4 is the main secreted product of the vertebrate thyroid gland and deiodination of its outer ring (ORD) produces the more active triiodo-l-thyronine (T 3 ), which has a much higher affinity for the thyroid hormone receptors (Leonard and Visser, 1986;Darras et al, 1998).…”

Section: Thyroid Gland and Hormonesmentioning

confidence: 99%

Evolution of the Thyroid Hormone-Binding Protein, Transthyretin

Power

Elias

Richardson

et al. 2000

General and Comparative Endocrinology

186

116

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Transthyretin (TTR) belongs to a group of proteins, which includes thyroxine-binding globulin and albumin, that bind to and transport thyroid hormones in the blood. TTR is also indirectly implicated in the carriage of vitamin A through the mediation of retinol-binding protein (RBP). It was first identified in 1942 in human serum and cerebrospinal fluid and was formerly called prealbumin for its ability to migrate faster than serum albumin on electrophoresis of whole plasma. It is a single polypeptide chain of 127 amino acids (14,000 Da) and is present in the plasma as a tetramer of noncovalently bound monomers. The major sites of synthesis of TTR in eutherian mammals, marsupials, and birds are the liver and choroid plexus but in reptiles it is synthesised only in the choroid plexus. The observation that TTR is strongly expressed in the choroid plexus but not in the liver of the stumpy-tailed lizard and the strong conservation of expression in the choroid plexus from reptiles to mammals have been taken as evidence to suggest that extrahepatic synthesis of TTR evolved first. The identification and cloning of TTR from the liver of an amphibian, Rana catesbeiana, and a teleost fish, Sparus aurata, and its absence from the choroid plexus of both species suggest an alternative model for its evolution. Protein modelling studies are presented that demonstrate differences in the electrostatic characteristics of the molecule in human, rat, chicken, and fish, which may explain why, in contrast to TTR from human and rat, TTR from fish and birds preferentially binds triiodo-L-thyronine.

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Control of Peripheral Thyroid Hormone Levels by Activating and Inactivating Deiodinases

Cited by 30 publications

References 18 publications

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Effects of Starvation and Refeeding on Gonadotropin and Thyrotropin Subunit mRNAs in Male Japanese Quail

Evolution of the Thyroid Hormone-Binding Protein, Transthyretin

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