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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
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Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Hyperthyroidism I: Introduction01:25

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Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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MTOR downregulates iodide uptake in thyrocytes.

Elaine Cristina Lima de Souza1, Alvaro Souto Padrón, William Miranda Oliveira Braga

  • 1Laboratório de Fisiologia Endócrina Doris Rosenthal, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

The Journal of Endocrinology
|April 16, 2010
PubMed
Summary

Mechanistic target of rapamycin (MTOR) inhibition boosts thyroid iodide uptake and sodium iodide symporter (NIS) expression. This kinase regulates normal thyroid cell function, with potential implications for thyroid cancer therapy.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cancer Research

Background:

  • Phosphoinositide-3-kinase (PI3K) signaling regulates cellular processes, including thyrocyte proliferation.
  • Mechanistic target of rapamycin (MTOR), a downstream effector of PI3K, is implicated in cellular metabolism, growth, and proliferation.
  • Thyroid stimulating hormone (TSH) activates MTOR, influencing thyrocyte behavior.

Purpose of the Study:

  • To investigate the role of MTOR in regulating thyroid iodide uptake and sodium iodide symporter (NIS) expression.
  • To determine if MTOR inhibition can enhance iodide uptake in thyroid cells.
  • To explore the therapeutic potential of MTOR inhibitors in thyroid function.

Main Methods:

  • Utilized FRTL-5 rat thyroid cell lines and papillary thyroid cancer cell lines.
  • Administered PI3K and MTOR inhibitors (rapamycin) to cell cultures.
  • Assessed iodide uptake and NIS protein expression.
  • Investigated the effects of TSH and insulin on these pathways.
  • Administered a rapamycin analog (everolimus) in vivo to rats.

Main Results:

  • MTOR inhibition by rapamycin increased iodide uptake in TSH-stimulated thyroid cells.
  • Insulin's downregulation of iodide uptake and NIS expression was counteracted by MTOR inhibition.
  • Rapamycin prevented TSH-induced activation of p70 S6 and AKT kinases, suggesting MTORC1/MTORC2 involvement.
  • Everolimus enhanced rat thyroid iodide uptake in vivo.

Conclusions:

  • MTOR kinase plays a significant role in controlling thyroid iodide uptake.
  • MTOR regulates not only cell survival but also normal thyroid cell function.
  • MTOR inhibition presents a potential strategy to enhance thyroid iodide uptake for therapeutic purposes.