Effects of Thyroid Hormone on Catecholamine and its Metabolite Concentrations in Rat Cardiac Muscle and Cerebral Cortex

Thyroid ◽  
1998 ◽  
Vol 8 (4) ◽  
pp. 353-358 ◽  
Author(s):  
TOSHIKI MANO ◽  
HIDEO SAKAMOTO ◽  
KO FUJITA ◽  
MASAKI MAKINO ◽  
HIROAKI KAKIZAWA ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Cardiac Muscle ◽  
Metabolite Concentrations

scholarly journals Thyroid Hormone Action in Cerebellum and Cerebral Cortex Development

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrice Chatonnet ◽  
Frédéric Picou ◽  
Teddy Fauquier ◽  
Frédéric Flamant
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Glial Cell ◽  
Nuclear Receptors ◽  
Target Genes ◽  
Cell Types ◽  
Hormone Action ◽  
Cerebral Cortex Development ◽  
Thyroid Hormone Action

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.

scholarly journals Thyroid Hormone Receptor β1 Expression in Developing Mouse Limbs and Face*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 1276-1281 ◽  
Author(s):  
Takeshi Nagasawa ◽  
Satoru Suzuki ◽  
Teiji Takeda ◽  
Leslie J. DeGroot
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Messenger Rna ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Urogenital Sinus ◽  
Blue Staining ◽  
Functional Study ◽  
Fetal Life ◽  
Amphibian Metamorphosis

Abstract Thyroid hormone, acting through thyroid hormone receptors (TRs), plays an important role in amphibian metamorphosis and vertebrate development. To identify where and when TRβ1 promoter is activated during fetal life, we carried out an in vivo functional study of a 1.3 kilobase (kb) TRβ1 gene promoter using transgenic mice that express the β-galactosidase gene under control of the TRβ1 promoter. Transactivation of the gene was determined by blue staining of tissues after incubation with X-gal. High expression of transgene was detected in the limbs and face of the 12.5-day-old fetus (12.5F) and 14.5F, reminiscent of the changes occurring during amphibian metamorphosis, and this disappeared at 17.5F. The expression was confined to the tip of finger bones, between fingers in the limb buds, and was detected in the root of whisker follicles, nose, and around the eyes. Signal was detected in the oral cavity, nasal cavity, lung, and urogenital sinus of 14.5F, and disappeared at 17.5F. Signal was detected in the midbrain and auditory vesicles of 9.5F but was reduced between 12.5F and 17.5F, and there was no expression in the cerebral cortex layer of 0 days old neonates (P0). Expression was detected in the cortex after P5. There was signal in the cerebral cortex, cerebellum, kidney, and liver of adult mice. TRβ1 messenger RNA was detected by RT-PCR in the developing limbs and face. Transgene expression in the interdigital tissues, which regress during development, suggests that TRβ1 is expressed in mammals in areas undergoing apoptosis as well as in areas undergoing differentiation.

scholarly journals Effect of thyroid hormone depletion on cultured murine cerebral cortex astrocytes

2009 ◽  
Vol 467 (2) ◽  
pp. 58-62 ◽  
Author(s):  
Rômulo Sperduto Dezonne ◽  
Joice Stipursky ◽  
Flávia Carvalho Alcantara Gomes
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone

scholarly journals Assessment of fecal steroid and thyroid hormone metabolites in eastern North Pacific gray whales

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Leila S Lemos ◽  
Amy Olsen ◽  
Angela Smith ◽  
Todd E Chandler ◽  
Shawn Larson ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
North Pacific ◽  
Reference Points ◽  
Future Research ◽  
Vital Rates ◽  
Baleen Whale ◽  
Gray Whales ◽  
Fecal Steroid ◽  
Metabolite Concentrations ◽  
The Impact

Abstract Baleen whale fecal samples have high potential for endocrine monitoring, which can be used as a non-invasive tool to identify the physiological response to disturbance events and describe population health and vital rates. In this study, we used commercial enzyme-linked immunosorbent assays to validate and quantify fecal steroid (progestins, androgens and glucocorticoids) and thyroid hormone metabolite concentrations in eastern North Pacific gray whales (Eschrichtius robustus) along the Oregon coast, USA, from May to October of 2016–2018. Higher mean progestin metabolite concentrations were observed in postweaning females, followed by pregnant females. Mean androgen, glucocorticoid and thyroid metabolites were higher in mature males. Progestin, glucocorticoids and thyroid fecal metabolites varied significantly by year, with positive correlations between progestin and androgen, and between glucocorticoid and thyroid metabolites. We also present two case studies of a documented injured whale and a mature male displaying reproductive competitive behavior, which provide reference points for physiologically stressed individuals and adult breeding males, respectively. Our methods and findings advance the knowledge of baleen whale physiology, can help guide future research on whale physiology and can inform population management and conservation efforts regarding minimizing the impact of anthropogenic stressors on whales.

scholarly journals Critical Role of Types 2 and 3 Deiodinases in the Negative Regulation of Gene Expression by T3 in the Mouse Cerebral Cortex

Endocrinology ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2919-2928 ◽  
Author(s):  
Arturo Hernandez ◽  
Beatriz Morte ◽  
Mónica M. Belinchón ◽  
Ainhoa Ceballos ◽  
Juan Bernal
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Critical Role ◽  
Regulation Of Gene Expression ◽  
Control Of Gene Expression ◽  
High Doses ◽  
And Function ◽  
Type 3

Thyroid hormones regulate brain development and function through the control of gene expression, mediated by binding of T3 to nuclear receptors. Brain T3 concentration is tightly controlled by homeostatic mechanisms regulating transport and metabolism of T4 and T3. We have examined the role of the inactivating enzyme type 3 deiodinase (D3) in the regulation of 43 thyroid hormone-dependent genes in the cerebral cortex of 30-d-old mice. D3 inactivation increased slightly the expression of two of 22 positively regulated genes and significantly decreased the expression of seven of 21 negatively regulated genes. Administration of high doses of T3 led to significant changes in the expression of 12 positive genes and three negative genes in wild-type mice. The response to T3 treatment was enhanced in D3-deficient mice, both in the number of genes and in the amplitude of the response, demonstrating the role of D3 in modulating T3 action. Comparison of the effects on gene expression observed in D3 deficiency with those in hypothyroidism, hyperthyroidism, and type 2 deiodinase (D2) deficiency revealed that the negative genes are more sensitive to D2 and D3 deficiencies than the positive genes. This observation indicates that, in normal physiological conditions, D2 and D3 play critical roles in maintaining local T3 concentrations within a very narrow range. It also suggests that negatively and positively regulated genes do not have the same physiological significance or that their regulation by thyroid hormone obeys different paradigms at the molecular or cellular levels.

Change in Thyroid Hormone Metabolite concentrations across Different Thyroid States

Thyroid ◽  
2021 ◽  
Author(s):  
Rutchanna M.S. Jongejan ◽  
Evert F.S. van Velsen ◽  
Marcel E Meima ◽  
Theo Klein ◽  
Sjoerd A.A. van den Berg ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Metabolite Concentrations

scholarly journals Hypothyroidism Decreases the Biogenesis in Free Mitochondria and Neuronal Oxygen Consumption in the Cerebral Cortex of Developing Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3953-3959 ◽  
Author(s):  
Bienvenida Martinez ◽  
Tiago B. Rodrigues ◽  
Elena Gine ◽  
John P. Kaninda ◽  
Ana Perez-Castillo ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Oxygen Consumption ◽  
Thyroid Hormone ◽  
Critical Role ◽  
Neural Population ◽  
Resonance Spectroscopy ◽  
13C Nuclear Magnetic Resonance ◽  
Respiratory Complex I ◽  
Flow Through

Thyroid hormone plays a critical role in mitochondrial biogenesis in two areas of the developing brain, the cerebral cortex and the striatum. Here we analyzed, in the cerebral cortex of neonatal rats, the effect of hypothyroidism on the biogenesis in free and synaptosomal mitochondria by analyzing, in isolated mitochondria, the activity of respiratory complex I, oxidative phosphorylation, oxygen consumption, and the expression of mitochondrial genome. In addition, we studied the effect of thyroid hormone in oxygen consumption in vivo by determining metabolic flow through 13C nuclear magnetic resonance spectroscopy. Our results clearly show that in vivo, hypothyroidism markedly reduces oxygen consumption in the neural population of the cerebral cortex. This effect correlates with decreased free mitochondria biogenesis. In contrast, no effect was observed in the biogenesis in synaptosomal mitochondria. The parameters analyzed were markedly improved after T3 administration. These results suggest that a reduced biogenesis and the subsequent reduction of respiratory capacity in free mitochondria could be the underlying cause of decreased oxygen consumption in the neurons of the cerebral cortex of hypothyroid neonates.

scholarly journals Fetal and Neonatal Iron Deficiency Reduces Thyroid Hormone-Responsive Gene mRNA Levels in the Neonatal Rat Hippocampus and Cerebral Cortex

Endocrinology ◽  
2012 ◽  
Vol 153 (11) ◽  
pp. 5668-5680 ◽  
Author(s):  
Thomas W. Bastian ◽  
Jeremy A. Anderson ◽  
Stephanie J. Fretham ◽  
Joseph R. Prohaska ◽  
Michael K. Georgieff ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Neonatal Rat ◽  
Fe Deficiency ◽  
Common Mechanism ◽  
Mrna Levels ◽  
Micronutrient Deficiencies ◽  
Sprague Dawley ◽  
Whole Brain ◽  
Responsive Gene

Abstract Copper (Cu), iron (Fe), and thyroid hormone (TH) deficiencies produce similar defects in late brain development including hypomyelination of axons and impaired synapse formation and function, suggesting that these micronutrient deficiencies share a common mechanism contributing to these derangements. We previously demonstrated that fetal/neonatal Cu and Fe deficiencies lower circulating TH concentrations in neonatal rats. Fe deficiency also reduces whole-brain T3 content, suggesting impaired TH action in the developing Fe-deficient brain. We hypothesized that fetal/neonatal Cu and Fe deficiencies will produce mild or moderate TH deficiencies and will impair TH-responsive gene expression in the neonatal cerebral cortex and hippocampus. To test this hypothesis, we rendered pregnant Sprague Dawley rats Cu-, Fe-, or TH-deficient from early gestation through postnatal d 10 (P10). Mild and moderate TH deficiencies were induced by 1 and 3 ppm propylthiouracil treatment, respectively. Cu deficiency did not significantly alter serum or tissue TH concentrations or TH-responsive brain mRNA expression. Fe deficiency significantly lowered P10 serum total T3 (45%), serum total T4 (52%), whole brain T3 (14%), and hippocampal T3 (18%) concentrations, producing a mild TH deficiency similar to 1 ppm propylthiouracil treatment. Fe deficiency lowered Pvalb, Enpp6, and Mbp mRNA levels in the P10 hippocampus. Fe deficiency also altered Hairless, Dbm, and Dio2 mRNA levels in the P10 cerebral cortex. These results suggest that some of the brain defects associated with Fe deficiency may be mediated through altered thyroidal status and the concomitant alterations in TH-responsive gene transcription.

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