scholarly journals Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development

2004 ◽  
Vol 180 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L Liu ◽  
TE Porter
Keyword(s):  
Thyroid Hormone ◽  
Embryonic Development ◽  
Thyroid Hormones ◽  
Synthesis Inhibitor ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Growth Hormone Cell ◽  
Thyroid Hormone Levels

Growth hormone cell differentiation normally occurs between day 14 and day 16 of chicken embryonic development. We reported previously that corticosterone (CORT) could induce somatotroph differentiation in vitro and in vivo and that thyroid hormones could act in combination with CORT to further augment the abundance of somatotrophs in vitro. The objective of the present study was to test our hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development. Plasma samples were collected on embryonic day (e) 9-14. We found that plasma CORT and thyroid hormone levels increased progressively in mid-embryogenesis to e 13 or e 14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e 11 increased somatotroph proportions prematurely on e 13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e 9 inhibited somatotroph differentiation in vivo, as assessed on e 14; this suppression was completely reversed by T3 replacement on e 11. Since we reported that T3 alone was ineffective in vitro, we interpret these findings to indicate that the effects of treatments in vivo were due to interactions with endogenous glucocorticoids. These results indicate that treatment with exogenous thyroid hormones can modulate somatotroph abundance and that endogenous thyroid hormone synthesis likely contributes to normal somatotroph differentiation.

scholarly journals N-Glycans Modulate in Vivo and in Vitro Thyroid Hormone Synthesis

1995 ◽  
Vol 270 (50) ◽  
pp. 29881-29888 ◽  
Author(s):  
Bernard Mallet ◽  
Pierre-Jean Lejeune ◽  
Nathalie Baudry ◽  
Patricia Niccoli ◽  
Pierre Carayon ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis

scholarly journals Acrylamide does not induce tumorigenesis or major defects in mice in vivo

2008 ◽  
Vol 198 (2) ◽  
pp. 301-307 ◽  
Author(s):  
Ling Jin ◽  
Vanessa Chico-Galdo ◽  
Claude Massart ◽  
Christine Gervy ◽  
Viviane De Maertelaere ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Chronic Administration ◽  
Serum Levels ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Thyroid Cells ◽  
Hormone Synthesis ◽  
Rat Thyroid

Chronic administration of acrylamide has been shown to induce thyroid tumors in rat. In vitro acrylamide also causes DNA damage, as demonstrated by the comet assay, in various types of cells including human thyroid cells and lymphocytes, as well as rat thyroid cell lines. In this work, mice were administered acrylamide in their drinking water in doses comparable with those used in rats, i.e., around 3–4 mg/kg per day for mice treated 2, 6, and 8 months. Some of the mice were also treated with thyroxine (T4) to depress the activity of the thyroid. Others were treated with methimazole that inhibits thyroid hormone synthesis and consequently secretion and thus induces TSH secretion and thyroid activation. These moderate treatments were shown to have their known effect on the thyroid (e.g. thyroid hormone and thyrotropin serum levels, thyroid gland morphology…). Besides, T4 induced an important polydipsia and degenerative hypertrophy of adrenal medulla. Acrylamide exerted various discrete effects and at high doses caused peripheral neuropathy, as demonstrated by hind-leg paralysis. However, it did not induce thyroid tumorigenesis. These results show that the thyroid tumorigenic effects of acrylamide are not observed in another rodent species, the mouse, and suggest the necessity of an epidemiological study in human to conclude on a public health policy.

scholarly journals Selective labelling and inactivation of creatine kinase isoenzymes by the thyroid hormone derivative N-bromoacetyl-3,3′,5-tri-iodo-l-thyronine

1993 ◽  
Vol 291 (2) ◽  
pp. 463-472 ◽  
Author(s):  
M Wyss ◽  
T Wallimann ◽  
J Köhrle
Keyword(s):  
Creatine Kinase ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Rat Heart ◽  
Covalent Modification ◽  
Regulation Of Transcription ◽  
Selective Labelling ◽  
Mitochondrial Fractions

Besides their well-known regulation of transcription by binding to nuclear receptors, thyroid hormones have been suggested to have direct effects on mitochondria. In a previous study, incubation of rat heart mitochondria with 125I-labelled N-bromoacetyl-3,3′,5-tri-iodo-L-thyronine (BrAcT3), a thyroid hormone derivative with an alkylating side chain, resulted in the selective labelling of a protein doublet around M(r) 45,000 on SDS/polyacrylamide gels [Rasmussen, Köhrle, Rokos and Hesch (1989) FEBS Lett. 255, 385-390]. Now, this protein doublet has been identified as mitochondrial creatine kinase (Mi-CK). Immunoblotting experiments with the cytoplasmic and mitochondrial fractions of rat heart, brain and liver, as well as inactivation studies with the purified chicken CK isoenzymes have further demonstrated that all four CK isoenzymes (Mia-, Mib-, M- and B-CK) are indeed selectively labelled by BrAcT3. However, in contrast with their bromoalkyl derivatives, thyroid hormones themselves did not compete for CK labelling, suggesting that not the thyroid hormone moiety but rather the bromoacetyl-driven alkylation of the highly reactive ‘essential’ thiol group of CK accounts for this selective labelling. Therefore the assumption that CK isoenzymes are thyroid-hormone-binding proteins has to be dismissed. Instead, bromoacetyl-based reagents may allow a very specific covalent modification and inactivation of CK isoenzymes in vitro and in vivo.

Effects of a selenium deficient diet on thyroid function of normal and perchlorate treated rats

1988 ◽  
Vol 118 (4) ◽  
pp. 495-502 ◽  
Author(s):  
J. Golstein ◽  
B. Corvilain ◽  
F. Lamy ◽  
D. Paquer ◽  
J. E. Dumont
Keyword(s):  
Thyroid Hormone ◽  
Tap Water ◽  
Selenium Deficiency ◽  
Thyroid Peroxidase ◽  
Deficient Diet ◽  
Adult Rats ◽  
Pregnant Rats ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis

Abstract. Pregnant rats were submitted to a selenium-deficient diet immediately after mating; it was continued for 4 weeks after delivery. The pups were sacrificed at 3 and 4 weeks of age. Perchlorate, an antithyroid agent inhibiting iodide trapping in the thyroid, was administered via the drinking water to half of the rats. Rats submitted to a normal laboratory diet and to the experimental diet supplemented with selenium were used as controls. The effects of selenium deficiency were an increase in the number of growth abnormalities, growth retardation, and decreased seleno-dependent glutathione peroxidase (GSH-Px) activity in plasma and in various organs. These effects were relieved by selenium supplementation in the diet. Perchlorate treatment induced the classic picture of primary hypothyroidism. Selenium deficiency increased thyroid hormone levels in perchlorate-treated rats and in controls drinking tap water. In the latter group, it also decreased TSH plasma concentration and thyroid weight. These effects were partially reversed by Se supplementation. In vitro experiments, performed on adult rats, revealed increased radioiodide uptake and organification in glands from the rats submitted to the selenium-free diet. Plasma T3 half-life was similar in control and Se-deficient rats. These data suggest a higher efficiency of thyroid hormone synthesis in the thyroids of selenium-deficient rats, despite a lower thyroid stimulation as evaluated by serum TSH. They are compatible with the hypothesis that decreased selenium supply, leading to a decreased GSH-Px in the thyroid, increases hydrogen peroxide steady state level and thus thyroid peroxidase activity and thyroid hormone synthesis.

In Vitro Measurements of Thyroid Hormones

1976 ◽  
Vol 62 (3) ◽  
pp. 169-172
Author(s):  
W. F. D. Sampson
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Laboratory Tests ◽  
Simple Manner ◽  
In Vitro Techniques ◽  
In Vitro Measurements ◽  
Considerable Confusion ◽  
Serum Thyroid Hormone ◽  
Thyroid Hormone Levels

AbstractConsiderable confusion among requesting physicians is often engendered by the multiplicity of laboratory tests of thyroid function. This paper seeks to set out in a simple manner the main in vitro techniques employed in this laboratory to measure serum thyroid hormone levels, their strengths and their weaknesses.

scholarly journals Extrathyroidal thyroid hormone synthesis?

2011 ◽  
Vol 210 (1) ◽  
pp. 3-4 ◽  
Author(s):  
Marian Ludgate
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis

A paper published in this issue of the Journal of Endocrinology has revisited the hypothesis that thyroid hormones may be generated by tissues outside the thyroid gland in higher organisms including mammals. This commentary appraises the strengths and weaknesses of the study, the alternative explanations for the findings and possible future measures to investigate further. The concept of extrathyroidal thyroxine and triiodothyronine synthesis has previously been proposed; by assuming that Nagao et al. and earlier authors are correct, the plausibility and possible mechanisms underlying the hypothesis are discussed.

Lack of refractoriness to stimulation with long acting thyroid stimulator of thyroid hormone synthesis and thyroid hormone secretion in mice in vivo

1983 ◽  
Vol 102 (3) ◽  
pp. 392-395 ◽  
Author(s):  
Hitoshi Ikeda ◽  
Shigenobu Nagataki
Keyword(s):  
Thyroid Hormone ◽  
Weight Control ◽  
Hormone Secretion ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Positive Serum ◽  
Ad Libitum ◽  
Long Acting ◽  
Prior Administration

Abstract. The present study was undertaken to examine whether long acting thyroid stimulator (LATS) induces refractoriness of thyroid hormone synthesis and thyroid hormone secretion to the stimulator in vivo. Male DDY mice fed with a low iodine diet and given 5 μg/ml of triiodothyronine (T3) in drinking water ad libitum for 4 days were injected with 0.25 ml of LATS positive serum (1000%/0.25 ml in the McKenzie bioassay) ip every 24 h for 9 days. Groups of 5 mice were sacrificed before and 1, 3, 5, 7 and 9 days after the first injection of LATS for the determinations of serum thyroxine (T4) concentrations, the 1 h thyroid 131I uptake and thyroid weight. Control mice were injected with LATS negative pooled normal sera. Serum T4 concentrations elevated significantly 24 h after the 3rd injection of LATS and remained elevated until the end of the experiment. One hour thyroid 131I uptake elevated about 3-fold 24 h after the first injection of LATS. It further increased 24 h after the 3rd injection of LATS to 10-fold of the value for control animals and stayed elevated at this same level for the remainder of the study. These results indicate that stimulating effects of LATS on thyroid hormone synthesis assessed by thyroid 131I uptake and thyroid hormone secretion assessed by serum T4 concentrations were not diminished by the prior administration of the stimulator. These findings suggest that LATS does not induce refractoriness of either thyroid hormone synthesis or thyroid hormone secretion to the stimulator in mice in vivo.

scholarly journals Production of Immunoreactive Thyroglobulin C-Terminal Fragments during Thyroid Hormone Synthesis

Endocrinology ◽  
2000 ◽  
Vol 141 (7) ◽  
pp. 2518-2525 ◽  
Author(s):  
Christine Duthoit ◽  
Valérie Estienne ◽  
Frédéric Delom ◽  
Josée-Martine Durand-Gorde ◽  
Bernard Mallet ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Monoclonal Antibodies ◽  
Free Radicals ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Fenton Reaction ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Generating System ◽  
Mediated Oxidation

Here, we studied the fragmentation of the prothyroid hormone, thyroglobulin (Tg), which occurs during thyroid hormone synthesis, a process which involves iodide, thyroperoxidase, and the H2O2-generating system, consisting of glucose and glucose oxidase. Various peptides were found to be immunoreactive to autoantibodies to Tg from patients and monoclonal antibodies directed against the immunodominant region of Tg. The smallest peptide (40 kDa) bore thyroid hormones and was identified at the C-terminal end of the Tg molecule, which shows homologies with acetylcholinesterase. Similar peptides were obtained by performing metal-mediated oxidation of Tg via a Fenton reaction. It was concluded that the oxidative stress induced during hormone synthesis generates free radicals, which, in turn, cleave Tg into immunoreactive peptides.

scholarly journals Thyroid Hormone Receptor α1 Directly Controls Transcription of the β-Catenin Gene in Intestinal Epithelial Cells

2006 ◽  
Vol 26 (8) ◽  
pp. 3204-3214 ◽  
Author(s):  
Michelina Plateroti ◽  
Elsa Kress ◽  
Jun Ichirou Mori ◽  
Jacques Samarut
Keyword(s):  
Thyroid Hormone ◽  
Epithelial Cell ◽  
Thyroid Hormones ◽  
Transcriptional Control ◽  
Thyroid Hormone Receptor ◽  
Intestinal Epithelial ◽  
Type D ◽  
Hormone Responsive Element

ABSTRACT Thyroid hormones, T3 and T4, are known regulators of intestine development. The best characterized example is the remodeling of the gastrointestinal tract during amphibian metamorphosis. Thyroid hormones act via nuclear receptors, the TRs, which are T3-dependent transcription factors. We previously showed that intestinal epithelial cell proliferation is controlled by thyroid hormones and the TRα gene. To analyze the mechanisms responsible, we studied the expression of genes belonging to and/or activated by the Wnt/β-catenin pathway, a major actor in the control of physiological and pathological epithelial proliferation in the intestine. We show that T3-TRα1 controls the transcription of the β-catenin gene in an epithelial cell-autonomous way. This is parallel to positive regulation of proliferation-controlling genes such as type D cyclins and c-myc, known targets of the Wnt/β-catenin. In addition, we show that the regulation of the β-catenin gene is direct, as TR binds in vitro and in chromatin in vivo to a specific thyroid hormone-responsive element present in intron 1 of this gene. This is the first report concerning in vivo transcriptional control of the β-catenin gene. As Wnt/β-catenin plays a crucial role in intestinal tumorigenesis, our observations open a new perspective on the study of TRs as potential tumor inducers.

scholarly journals ZFP36L2 Role in Thyroid Functionality

2021 ◽  
Vol 22 (17) ◽  
pp. 9379
Author(s):  
Francesco Albano ◽  
Valeria Tucci ◽  
Perry J. Blackshear ◽  
Carla Reale ◽  
Luca Roberto ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Specific Gene ◽  
In Vivo Models ◽  
Knock Out ◽  
Hormone Synthesis ◽  
And Function ◽  
Genetically Determined ◽  
Thyroid Development

Thyroid hormone levels are usually genetically determined. Thyrocytes produce a unique set of enzymes that are dedicated to thyroid hormone synthesis. While thyroid transcriptional regulation is well-characterized, post-transcriptional mechanisms have been less investigated. Here, we describe the involvement of ZFP36L2, a protein that stimulates degradation of target mRNAs, in thyroid development and function, by in vivo and in vitro gene targeting in thyrocytes. Thyroid-specific Zfp36l2-/- females were hypothyroid, with reduced levels of circulating free Thyroxine (cfT4) and Triiodothyronine (cfT3). Their hypothyroidism was due to dyshormonogenesis, already evident one week after weaning, while thyroid development appeared normal. We observed decreases in several thyroid-specific transcripts and proteins, such as Nis and its transcriptional regulators (Pax8 and Nkx2.1), and increased apoptosis in Zfp36l2-/- thyroids. Nis, Pax8, and Nkx2.1 mRNAs were also reduced in Zfp36l2 knock-out thyrocytes in vitro (L2KO), in which we confirmed the increased apoptosis. Finally, in L2KO cells, we showed an altered response to TSH stimulation regarding both thyroid-specific gene expression and cell proliferation and survival. This result was supported by increases in P21/WAF1 and p-P38MAPK levels. Mechanistically, we confirmed Notch1 as a target of ZFP36L2 in the thyroid since its levels were increased in both in vitro and in vivo models. In both models, the levels of Id4 mRNA, a potential inhibitor of Pax8 activity, were increased. Overall, the data indicate that the regulation of mRNA stability by ZFP36L2 is a mechanism that controls the function and survival of thyrocytes.

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