scholarly journals Ontogenic Redistribution of Type 2 Deiodinase Messenger Ribonucleic Acid in the Brain of Chicken

Endocrinology ◽  
2004 ◽  
Vol 145 (8) ◽  
pp. 3619-3625 ◽  
Author(s):  
Balázs Gereben ◽  
Janusz Pachucki ◽  
Anna Kollár ◽  
Zsolt Liposits ◽  
Csaba Fekete
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Hormone Receptors ◽  
Third Ventricle ◽  
Hybridization Signal ◽  
Adult Chicken ◽  
Chicken Brain ◽  
Messenger Ribonucleic Acid ◽  
The Brain

Abstract Thyroid hormone is essential for brain development. T4 has to be converted to T3 for efficient binding to thyroid hormone receptors. Type 2 deiodinase (D2) is the key enzyme that allows T3 generation in the brain. To elucidate the onset and localization of T3 production in the brain, we studied the changes of D2 activity, mRNA content, and the distribution of D2 mRNA in the brain of chicken embryos before and after the onset of thyroid function. D2 activity was detectable in the brain at all stages studied from embryonic day (E)7 to E15 and increased significantly with time. The wild-type chicken D2 transcript was detectable at all those stages by RT-PCR. The amount of D2 mRNA in the brain increased approximately 14-fold from E10 to E17 as assessed by Northern blot. Week D2 hybridization signal could be detected by in situ hybridization at E8 in cell clusters throughout the brain, and its intensity markedly increased to E15. Interestingly, no D2 expression was detected in hypothalamic tanycytes at these embryonic stages. However, D2 hybridization signal was observed in the wall of the third ventricle of adult chicken posterior to the rostral pole of the median eminence in the location typical for tanycytes, whereas D2 signal in other localizations was decreased throughout the brain. Our data suggest that D2 contributes to T3 content of the developing chicken brain even before the onset of thyroid function. Furthermore, redistribution of D2 mRNA expression was observed during the development of the chicken brain.

scholarly journals Thyroid Hormone and the Neuroglia: Both Source and Target

2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Petra Mohácsik ◽  
Anikó Zeöld ◽  
Antonio C. Bianco ◽  
Balázs Gereben
Keyword(s):  
Thyroid Hormone ◽  
Cell Function ◽  
Hormone Regulation ◽  
Mediobasal Hypothalamus ◽  
Iodothyronine Deiodinase ◽  
Neuronal Gene ◽  
Health And Disease ◽  
And Function ◽  
The Brain

Thyroid hormone plays a crucial role in the development and function of the nervous system. In order to bind to its nuclear receptor and regulate gene transcription thyroxine needs to be activated in the brain. This activation occurs via conversion of thyroxine to T3, which is catalyzed by the type 2 iodothyronine deiodinase (D2) in glial cells, in astrocytes, and tanycytes in the mediobasal hypothalamus. We discuss how thyroid hormone affects glial cell function followed by an overview on the fine-tuned regulation of T3 generation by D2 in different glial subtypes. Recent evidence on the direct paracrine impact of glial D2 on neuronal gene expression underlines the importance of glial-neuronal interaction in thyroid hormone regulation as a major regulatory pathway in the brain in health and disease.

scholarly journals Thyroid Hormone Changes Related to Growth Hormone Therapy in Growth Hormone Deficient Patients

2021 ◽  
Vol 10 (22) ◽  
pp. 5354
Author(s):  
Anna Małgorzata Kucharska ◽  
Ewelina Witkowska-Sędek ◽  
Małgorzata Rumińska ◽  
Beata Pyrżak
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormone ◽  
Thyroid Function ◽  
Hormone Receptors ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Hormone Deficiency ◽  
Central Hypothyroidism ◽  
Rhgh Therapy ◽  
The Impact

The alterations in thyroid function during recombinant human growth hormone (rhGH) treatment have been reported by many authors since this therapy became widely available for patients with growth hormone deficiency (GHD). Decrease of thyroxine level is the most frequent observation in patients treated with rhGH. This paper presents literature data describing changes in thyroid function related to rhGH therapy and a current explanation of mechanisms involved in this phenomenon. The effect of GH on the hypothalamic-pituitary-thyroid (HPT) axis is dependent on a multilevel regulation beginning from influence on the central axis, thyroid, and extra-thyroidal deiodinases activity as well as the impact on thyroid hormone receptors on the end. Changes in central and peripheral regulation could overlap during rhGH therapy, resulting in central hypothyroidism or an isolated slight deficiency of thyroxine. The regular monitoring of thyroid function is recommended in patients treated with rhGH and the decision of levothyroxine (L-thyroxine) supplementation should be made in the clinical context, taking into account thyroid hormone levels, as well as the chance for satisfactory growth improvement.

scholarly journals Correlation Between the Thyroid Hormone Levels and Nonalcoholic Fatty Liver Disease in Type 2 Diabetic Patients with Normal Thyroid Function

2020 ◽  
Author(s):  
Yuanyuan Zhang ◽  
Huaizhen Liu ◽  
Juyi Li ◽  
Ling Li ◽  
Jinjun Zhang ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Liver Fibrosis ◽  
Thyroid Function ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Normal Thyroid ◽  
Hormone Levels ◽  
Normal Thyroid Function ◽  
Thyroid Hormone Levels

Abstract Background: The objective of this study is to retrospectively analyze the correlation between the thyroid hormones and nonalcoholic fatty liver disease (NAFLD) in type 2 diabetes mellitus (T2DM) patients with normal thyroid function. Methods: Totally 586 T2DM patients with normal thyroid function participated in this research and were divided into T2DM without NAFLD (240 cases) group and T2DM with NAFLD (346 cases) group. The NAFLD fibrosis score (NFS) >0.676 was defined as progressive liver fibrosis and used to categorize the patients into T2DM without progressive liver fibrosis group (493 cases) and T2DM with progressive liver fibrosis group (93 cases). Results: The results indicated that the levels of free triiodothyronine (FT3) and total triiodomethylamine (TT3) were significantly higher while the free thyroxine (FT4) level was lower in T2DM with NAFLD group than that in T2DM2 without NAFLD group (p<0.05). The levels of FT3, FT4 and TT3 in patients with progressive liver fibrosis were significantly lower in patients with progressive liver fibrosis than that in patients without progressive liver fibrosis (p<0.05). Logistic regression analysis showed a negative relationship between FT4 level and NAFLD (p=0.026), between the levels of FT4,TT3 and total thyroxine (TT4) and the risk of progressive hepatic fibrosis (p=0.022, p=0.007,p=0.046).Conclusion: There is a certain correlation between thyroid hormone levels and NAFLD in T2DM patients, suggesting that the assessment of thyroid hormone levels in T2DM patients with normal thyroid function is of great significance in the prevention and treatment of NAFLD.

Transient embryonic antigens in the chick

Development ◽  
1964 ◽  
Vol 12 (3) ◽  
pp. 511-516
Author(s):  
D. J. McCallion ◽  
J. C. Trott
Keyword(s):  
Spinal Cord ◽  
Chick Embryo ◽  
Primitive Streak ◽  
Adult Chicken ◽  
Tissue Specific ◽  
Chicken Brain ◽  
Early Chick Embryo ◽  
Embryonic Antigens ◽  
Specific Antigens ◽  
The Brain

The Presence of an organ antigen in the early chick embryo was first demonstrated by Schechtman (1948). He found that an antigenic substance common to brain, heart, liver and muscle of chicks at hatching is already present in primitive streak and early neurula stages of the embryo. This observation, with respect to brain and heart, was subsequently confirmed by Ebert (1950). McCallion & Langman (1964) have recently demonstrated that there are at least eight antigenic substances in the adult chicken brain that are class-specific but that are more or less common to other organs, with only quantitative differences. These authors have further demonstrated that there are at least three, possibly as many as five, antigenic substances in adult chicken brain that are not only class-specific but also tissue-specific, occurring only in the brain, spinal cord, nervous retina and nerves. The non-specific antigens appear progressively during the first 4 days of incubation.

scholarly journals Thyroid Hormone Homeostasis and Action in the Type 2 Deiodinase-Deficient Rodent Brain during Development

Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3080-3088 ◽  
Author(s):  
Valerie Anne Galton ◽  
Emily T. Wood ◽  
Emily A. St. Germain ◽  
Cheryl-Ann Withrow ◽  
George Aldrich ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Indirect Evidence ◽  
Wild Type Mouse ◽  
Brown Fat ◽  
Current View ◽  
Mrna Levels ◽  
Compensatory Mechanisms ◽  
Hormone Homeostasis ◽  
The Brain

Considerable indirect evidence suggests that the type 2 deiodinase (D2) generates T3 from T4 for local use in specific tissues such as pituitary, brown fat, and brain, and studies with a D2-deficent mouse, the D2 knockout (D2KO) mouse, have shown this to be the case in pituitary and brown fat. The present study employs the D2KO mouse to determine the role of D2 in the developing brain. As expected, the T3 content in the neonatal D2KO brain was markedly reduced to a level comparable with that seen in the hypothyroid neonatal wild-type mouse. However, the mRNA levels of several T3-responsive genes were either unaffected or much less affected in the brain of the D2KO mouse than in that of the hypothyroid mouse, and compared with the hypothyroid mouse, the D2KO mouse exhibited a very mild neurological phenotype. The current view of thyroid hormone homeostasis in the brain dictates that the T3 present in neurons is generated mostly, if not exclusively, from T4 by the D2 in glial cells. This view is inadequate to explain the findings presented herein, and it is suggested that important compensatory mechanisms must be in play in the brain to minimize functional abnormalities in the absence of the D2.

scholarly journals Thyroid function and effect of aging in combined hetero/homozygous mice deficient in thyroid hormone receptors alpha and beta genes

2002 ◽  
Vol 172 (1) ◽  
pp. 177-185 ◽  
Author(s):  
RE Weiss ◽  
O Chassande ◽  
EK Koo ◽  
PE Macchia ◽  
K Cua ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors ◽  
Thyroid Function Tests ◽  
Wild Type ◽  
Heterozygous Mouse ◽  
Tsh Secretion ◽  
Homozygous Deletions ◽  
Serum Tsh

The maintenance of thyroid hormone (TH) homeostasis is dependent on the synthesis and secretion of TH regulated by TSH. This is achieved, in turn, by the negative feedback of TH on TSH secretion and synthesis, which requires the interaction with TH receptors (TRs). Derived by alternative splicing of two gene transcription products, three TRs (TRbeta1, TRbeta2 and TRalpha1) interact with TH while another, TRalpha2, binds to DNA but not to TH. In this study we compare the results of thyroid function tests in mice with deletions of the TRalpha and TRbeta genes alone and present novel data on mice that are double homozygous and combined heterozygous. Homozygous deletions of both the TRalpha and TRbeta in the same mouse (TRalphao/o; TRbeta-/-) resulted in serum TSH values only slightly lower than those in athyreotic, Pax8 knockout mice. Whereas the absence of TRalpha alone does not cause resistance to TH, the absence of TRbeta in the presence of TRalpha results in a 205, 169, 544% increase in serum thyroxine (T(4)), triiodothyronine (T(3)) and TSH concentrations respectively. However, in the absence of TRbeta, loss of one TRalpha allele can worsen the resistance to TH with a 243 and 307% increase in T(4) and T(3) respectively. Similarly, while the heterozygous mouse with a single TRbeta allele shows no alteration in thyroid function, the concomitant deletion of TRalpha brings about mild but significant resistance to TH. Furthermore, the severity of the resistance to TH was noted to decrease with age in parallel with the decrease in serum free T(4) values also seen in wild-type mice. These results demonstrate that (1) unliganded TRalpha or TRbeta are not absolutely necessary for the upregulation of TSH; (2) TRbeta but not TRalpha is sufficient for TH-mediated downregulation of TSH; and (3) TRalpha may partially substitute for TRbeta in mediating a partial TH-dependent TSH suppression.

Biosynthesis, transport, metabolism, and actions of thyroid hormones

2011 ◽  
pp. 307-321
Author(s):  
Theo J. Visser
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Iodine Intake ◽  
Thyroid Stimulating Hormone ◽  
Thyroid State ◽  
Peripheral Tissues ◽  
Healthy Humans ◽  
Inactive Metabolite ◽  
Tsh Secretion ◽  
The Brain

In healthy humans with a normal iodine intake, the thyroid follicular cells produce predominantly the prohormone thyroxine (3,3′,5,5′-tetraiodothyronine; T4), which is converted in peripheral tissues to the bioactive hormone 3,3′,5-triiodothyronine (T3) or to the inactive metabolite 3,3′,5′-triiodothyronine (reverse T3). The bioavailability of thyroid hormone in target tissues depends to a large extent on the supply of plasma T4 and T3, the activity of transporters mediating the cellular uptake and/or efflux of these hormones, as well as the activity of deiodinases and possibly other enzymes catalyzing their activation or inactivation. Thyroid function is regulated most importantly by the hypophyseal glycoprotein thyroid-stimulating hormone (TSH), also called thyrotropin. In turn, TSH secretion from the anterior pituitary is stimulated by the hypothalamic factor thyrotropin-releasing hormone (TRH). TSH secretion is down-regulated by negative feedback action of thyroid hormone on the hypothalamus and the pituitary. The contribution of locally produced T3 versus uptake of plasma T3 is much greater for some tissues such as the brain and the pituitary than for most other tissues. Plasma TSH is an important parameter for the diagnosis of thyroid dysfunction but is not representative for the thyroid state of all tissues. In this chapter various aspects will be discussed of: (a) the neuroendocrine regulation of thyroid function, (b) the biosynthesis of thyroid hormone (i.e. the prohormone T4), (c) the activation and inactivation of thyroid hormone in peripheral tissues, and (d) the mechanism by which T3 exerts it biological activity. A schematic overview of the hypothalamus– pituitary–thyroid–periphery axis is presented in Fig. 3.1.2.1.

scholarly journals Ontogeny, regional distribution and properties of thyroid-hormone receptors in the developing chick brain

1984 ◽  
Vol 220 (2) ◽  
pp. 547-552 ◽  
Author(s):  
M A Haidar ◽  
P K Sarkar
Keyword(s):  
Thyroid Hormone ◽  
Embryonic Development ◽  
Hormone Receptors ◽  
Late Phase ◽  
Regional Distribution ◽  
Endogenous Hormone ◽  
Thyroid Hormone Receptors ◽  
Chick Brain ◽  
Receptor Complexes ◽  
The Brain

Studies on the thyroid-hormone receptors in the nuclei of developing chick brain revealed a single class of binding sites for tri-iodothyronine (T3) and thyroxine (T4) at all embryonic and adult ages. High-affinity [Ka = (1.85-3.3) X 10(9)M-1 and (0.3-0.6 × 10(9)M-1 for T3 and T4 respectively] receptors were detected in the brain as early as day 7 of embryonic development; their level increased progressively rapidly until day 13, and thereafter the value remained essentially constant during development. Occupancy of the receptor site with endogenous hormone was 75-90% at 7-11 days, 50-60% during the late phase of embryogenesis (13-17 days), and 80% after hatching. Comparison of the binding properties of the receptors with T3 and T4 indicates that, although the binding capacities per nucleus are almost identical, T4 has four to five times less binding affinity than T3. The half-lives of dissociation of solubilized T3- receptor complexes were 20-30h between 0 degrees and 7 degrees C, about 4h at 20 degrees C and less than 15 min at 37 degrees C. Studies of the regional distribution of receptors in the brain indicate that cerebrum has the highest concentration of T3 receptors (4000-7000 sites per nucleus); this concentration is 2-4-fold higher than that in the cerebellum, optic lobe or medulla oblongata. The overall results indicate that between 7 and 13 days of embryonic development the thyroid-hormone receptors in the embryonic chick brain, particularly in the cerebrum, assume a very high level and appear to be mostly saturated with endogenous hormone. This, and the temporal correspondence of the phenomenon with the period of neuronal growth and synaptogenesis, strongly indicate the influence of the hormone in the maturation of the developing brain.

Sign in / Sign up

Export Citation Format

Share Document