Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Synthesis and Regulation of Thyroid Hormones

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...

Functions of Thyroid Hormones

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.
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...

Hyperthyroidism I: Introduction

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: Pathophysiology

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 II: Pathophysiology

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: Pathophysiology

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

Association between residual thyroid carcinoma and diffuse hepatic uptake of 131I following radioiodine ablation in postoperative total thyroidectomy patients.

World journal of surgery·2001

Same author

A comparison of recombinant human thyrotropin and thyroid hormone withdrawal for the detection of thyroid remnant or cancer.

The Journal of clinical endocrinology and metabolism·1999

Same author

Thyroid hormone export in rat FRTL-5 thyroid cells and mouse NIH-3T3 cells is carrier-mediated, verapamil-sensitive, and stereospecific.

Endocrinology·1999

Same author

Evidence for an ATP-dependent bile acid transport protein other than the canalicular liver ecto-ATPase in rats.

Gastroenterology·1997

Same author

Nuclear imaging in the management of thyroid carcinoma.

Thyroid : official journal of the American Thyroid Association·1996

Same author

Thyroid hormone export regulates cellular hormone content and response.

The Journal of biological chemistry·1996

Search research articles

Related Experiment Video

Updated: Jul 24, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Iodine metabolism and thyroid physiology: current concepts

R R Cavalieri¹

¹Nuclear Medicine Service, VA Medical Center, San Francisco, California, USA.

Thyroid : Official Journal of the American Thyroid Association

|April 1, 1997

Summary

Recent advances in thyroid physiology include the cloning of the thyroid iodine transporter and the discovery of a specific mechanism for triiodothyronine (T3) efflux from cells, impacting thyroid hormone action.

Area of Science:

Endocrinology
Molecular Biology
Physiology

Background:

Iodine is crucial for thyroid hormone synthesis and thyroid gland regulation.
Thyroid hormone (TH) transport and cellular uptake involve complex mechanisms.
Recent research has clarified key aspects of thyroid physiology.

Purpose of the Study:

To review recent advances in thyroid physiology, focusing on iodine transport and TH regulation.
To highlight the cloning of the thyroid iodine transporter and its implications.
To elucidate the mechanisms of cellular triiodothyronine (T3) efflux.

Main Methods:

Review of recent scientific literature.
Cloning of the thyroid iodine transporter.
Studies on cellular T3 efflux mechanisms.

More Related Videos

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Colorimetric Assessment of Deiodinase 1 Activity in Human Liver Microsomes Using the Sandell-Kolthoff Reaction

Colorimetric Assessment of Deiodinase 1 Activity in Human Liver Microsomes Using the Sandell-Kolthoff Reaction

Published on: April 10, 2026

Related Experiment Videos

Last Updated: Jul 24, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Colorimetric Assessment of Deiodinase 1 Activity in Human Liver Microsomes Using the Sandell-Kolthoff Reaction

Colorimetric Assessment of Deiodinase 1 Activity in Human Liver Microsomes Using the Sandell-Kolthoff Reaction

Published on: April 10, 2026

Main Results:

The thyroid iodine transporter has been cloned, enabling further study of iodine uptake regulation.
TSH regulates iodine uptake in the thyroid gland, unlike in other organs.
A specific, saturable, verapamil-inhibitable mechanism for T3 efflux from cells has been identified.

Conclusions:

The cloning of the thyroid iodine transporter is a major breakthrough for understanding thyroid function and disease.
Cellular T3 efflux is an active, regulated process that influences TH action.
These findings advance our understanding of thyroid hormone homeostasis and signaling.