Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effect on bone mineralization of continued growth hormone therapy at the transition between childhood and adulthood.

Endocrine connections·2026
Same author

Adherence and quality of life in children receiving rhGH treatment.

Archives de pediatrie : organe officiel de la Societe francaise de pediatrie·2023
Same author

Evaluation of auditory pathway excitability using a pre-operative trans-tympanic electrically evoked auditory brainstem response under local anesthesia in cochlear implant candidates.

International journal of audiology·2022
Same author

Neonatal screening for congenital hypothyroidism: Time to lower the TSH threshold in France.

Archives de pediatrie : organe officiel de la Societe francaise de pediatrie·2022
Same author

Novel method of fitting of children with auditory brainstem implants.

European annals of otorhinolaryngology, head and neck diseases·2018
Same author

Impact of transitional care on endocrine and anthropometric parameters in Prader-Willi syndrome.

Endocrine connections·2018

Related Experiment Video

Updated: Jul 1, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Hyperfunctioning thyroid adenoma and activating mutations in the TSH receptor gene.

M Polak1

  • 1Service d'endocrinologie et de diabétologie pédiatriques (Pr Czernichow), Paris, France. michel.polak@rdb.ap-hop-paris.fr

Archives of Medical Research
|March 14, 2000
PubMed
Summary

Constitutively active TSH receptor mutations drive toxic thyroid adenomas and hot nodules. Low iodine intake exacerbates these mutations, revealing insights into thyroid receptor physiology and autonomy.

More Related Videos

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Related Experiment Videos

Last Updated: Jul 1, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Thyroid Research

Background:

  • Thyrotropin (TSH) regulates thyrocyte function, differentiation, and growth via the TSH receptor and cyclic AMP mechanisms.
  • Constitutive activation of the TSH receptor, analogous to adrenergic receptor data, was hypothesized to cause autonomous thyroid function.

Purpose of the Study:

  • To investigate the role of TSH receptor mutations in thyroid autonomy.
  • To elucidate the molecular mechanisms underlying toxic thyroid adenomas and hot nodules.

Main Methods:

  • Analysis of TSH receptor mutations.
  • Correlation of mutation presence with thyroid nodule function (toxic adenomas, hot nodules).
  • Assessment of iodine supply's influence on mutation expression.

Main Results:

  • TSH receptor mutations leading to constitutive activation are the primary cause of toxic thyroid adenomas.
  • The same mechanism underlies "hot" thyroid nodules in multinodular goiter.
  • Low iodine supply amplifies the clinical manifestation of these somatic mutations.

Conclusions:

  • TSH receptor mutations are key drivers of thyroid autonomy.
  • A model for TSH receptor physiology is proposed where the unliganded receptor exerts negative control, while mutations lead to constitutive activation.
  • Understanding these mutations provides insights into thyroid disease pathogenesis.