Jove
Visualize
Contact Us

Related Concept Videos

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...
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...
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...
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...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Iodotyrosines Are Biomarkers for Preclinical Stages of Iodine-Deficient Hypothyroidism in <i>Dehal1</i>-Knockout Mice.

Thyroid : official journal of the American Thyroid Association·2023
Same author

Thyroid hormone regulators in human cerebral cortex development.

The Journal of endocrinology·2022
Same author

Single-Cell Transcriptome Profiling of Thyroid Hormone Effectors in the Human Fetal Neocortex: Expression of <i>SLCO1C1</i>, <i>DIO2</i>, and <i>THRB</i> in Specific Cell Types.

Thyroid : official journal of the American Thyroid Association·2021
Same author

Brain Gene Expression in Systemic Hypothyroidism and Mouse Models of MCT8 Deficiency: The Mct8-Oatp1c1-Dio2 Triad.

Thyroid : official journal of the American Thyroid Association·2020
Same author

Prenatal Treatment of Thyroid Hormone Cell Membrane Transport Defect Caused by <i>MCT8</i> Gene Mutation.

Thyroid : official journal of the American Thyroid Association·2020
Same author

Identification of Resistance to Exogenous Thyroxine in Humans.

Thyroid : official journal of the American Thyroid Association·2020
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 Experiment Video

Updated: Jun 3, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

[Thyroid hormone resistance syndromes].

Juan Bernal1

  • 1Instituto de Investigaciones Biomédicas, CSIC-UAM y CIBER de enfermedades raras, Madrid, España. jbernal@iib.uam.es

Endocrinologia Y Nutricion : Organo De La Sociedad Espanola De Endocrinologia Y Nutricion
|April 5, 2011
PubMed
Summary
This summary is machine-generated.

Thyroid hormone resistance syndromes involve genetic conditions with reduced tissue sensitivity to thyroid hormones. This review covers resistance due to receptor mutations, transport issues, or impaired conversion, discussing mechanisms and clinical strategies.

Related Experiment Videos

Last Updated: Jun 3, 2026

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
  • Genetics
  • Molecular Biology

Background:

  • Thyroid hormone resistance syndromes (THRS) are rare genetic disorders.
  • Characterized by decreased tissue sensitivity to thyroid hormones (T4 and T3).
  • Impacts metabolism, growth, and development.

Purpose of the Study:

  • Provide an updated review of THRS.
  • Discuss pathogenetic mechanisms of different resistance forms.
  • Outline clinical approaches for managing THRS.

Main Methods:

  • Literature review of genetic mutations affecting thyroid hormone action.
  • Analysis of transport and deiodinase pathways involved in thyroid hormone metabolism.
  • Synthesis of clinical data and therapeutic strategies.

Main Results:

  • Identified three main forms of THRS: TRβ gene mutations, impaired T4/T3 transport, and defective deiodinase activity.
  • Detailed pathogenetic mechanisms for each form.
  • Summarized current clinical diagnostic and management approaches.

Conclusions:

  • THRS encompass diverse genetic defects impacting thyroid hormone signaling.
  • Accurate diagnosis relies on understanding specific molecular defects.
  • Tailored clinical management is essential for improving patient outcomes.