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

9.5K
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...
9.5K
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

6
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...
6
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

7.1K
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.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
7.1K
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

4
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...
4
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

4
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...
4
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

5
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,...
5

You might also read

Related Articles

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

Sort by
Same author

A Longitudinal, Real-World Study of the Relationship between Levothyroxine Dose and Suboptimal Hypothyroidism Treatment.

Thyroid : official journal of the American Thyroid Association·2026
Same author

Impact of Hypothyroidism on Short-Term and Long-Term Outcomes of Coronary Artery Bypass Graft Surgery.

Thyroid : official journal of the American Thyroid Association·2026
Same author

A Phase 2 Study of XP-8121: Once-Weekly Subcutaneous Levothyroxine Sodium for the Treatment of Hypothyroidism in Adults.

Thyroid : official journal of the American Thyroid Association·2026
Same author

Overnutrition in mice impairs thyroid hormone biosynthesis and utilization, causing hypothyroidism, despite remarkable thyroidal adaptations.

The Journal of clinical investigation·2026
Same author

Thyroid Hormone Synthesis Without Thyroglobulin.

Thyroid : official journal of the American Thyroid Association·2026
Same author

Measuring deiodinase activity: a need for standardization?

European thyroid journal·2026

Related Experiment Video

Updated: Apr 19, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

2.7K

Differences in hypothalamic type 2 deiodinase ubiquitination explain localized sensitivity to thyroxine.

Joao Pedro Werneck de Castro, Tatiana L Fonseca, Cintia B Ueta

    The Journal of Clinical Investigation
    |January 3, 2015
    PubMed
    Summary

    Levothyroxine (L-T4) therapy for hypothyroidism can lead to low triiodothyronine (T3) levels. Tissue-specific differences in deiodinase (D2) activity, particularly in the hypothalamus, explain this imbalance and the high thyroxine/T3 ratio.

    More Related Videos

    Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
    04:14

    Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model

    Published on: October 6, 2023

    1.4K
    In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
    11:36

    In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

    Published on: July 25, 2019

    11.6K

    Related Experiment Videos

    Last Updated: Apr 19, 2026

    Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
    04:39

    Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

    Published on: March 17, 2023

    2.7K
    Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
    04:14

    Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model

    Published on: October 6, 2023

    1.4K
    In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
    11:36

    In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

    Published on: July 25, 2019

    11.6K

    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Neuroscience

    Background:

    • Current hypothyroidism treatment with levothyroxine (L-T4) normalizes thyroid-stimulating hormone (TSH) but often results in low serum 3,5,3'-triiodothyronine (T3) and a high thyroxine/T3 (T4/T3) ratio.
    • The brain, particularly the hypothalamus, relies on locally generated T3 from T4 conversion via type 2 deiodinase (D2), a process regulated by WSB-1-mediated ubiquitination.

    Purpose of the Study:

    • To investigate the role of tissue-specific differences in D2 ubiquitination in causing the high T4/T3 ratio observed in L-T4 treated hypothyroid rats.
    • To understand the impact of L-T4 on D2 activity and T3 generation in the hypothalamus compared to other tissues.

    Main Methods:

    • Studied thyroidectomized (Tx) rats with subcutaneous L-T4 pellets to assess serum hormone levels and D2 activity.
    • Utilized astrocyte-specific Wsb1 deletion mouse models and in vitro tissue extracts to analyze D2 ubiquitination patterns.

    Main Results:

    • L-T4 treatment reduced whole-body T4 to T3 conversion but minimally affected hypothalamic D2 activity.
    • Hypothalamic D2 ubiquitination was found to be relatively lower, leading to increased hypothalamic sensitivity to T4.
    • These findings highlight tissue-specific regulation of D2 activity as a key factor in thyroid hormone homeostasis.

    Conclusions:

    • Tissue-specific differences in D2 ubiquitination are integral to the hypothalamic-pituitary-thyroid axis feedback regulation.
    • Constant delivery of both L-T4 and L-T3 is necessary to fully normalize T3-dependent metabolic markers and gene expression in thyroidectomized rats.