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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...
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...
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...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

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Related Experiment Video

Updated: May 28, 2026

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

Thyroid iodide efflux: a team effort?

Peying Fong1

  • 1Department of Anatomy and Physiology, Kansas State University College of Veterinary Medicine, Manhattan, KS 66506, USA. pfong@vet.k-state.edu

The Journal of Physiology
|October 12, 2011
PubMed
Summary
This summary is machine-generated.

Thyroid hormones (T4 and T3) require iodide for synthesis. New evidence questions Pendrin as the sole iodide transporter, suggesting other channels like CLC-5, CFTR, and SMCT1 may be involved in thyroid iodide uptake.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

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Last Updated: May 28, 2026

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

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
  • Cell Physiology

Background:

  • Thyroid hormones thyroxine (T4) and triiodothyronine (T3) are crucial for development, growth, and metabolism.
  • Iodide (I-) is essential for thyroid hormone synthesis and is actively accumulated by the thyroid gland.
  • Environmental iodide scarcity necessitates efficient thyroid transport mechanisms for hormone production.

Purpose of the Study:

  • To re-evaluate the mechanisms of iodide transport in thyroid follicular epithelial cells.
  • To investigate alternative iodide (I-) transport pathways beyond the known Pendrin (SLC26A4) transporter.
  • To identify potential roles of CLC-5, CFTR, and SMCT1 in thyroidal iodide translocation.

Main Methods:

  • Review of recent evidence regarding iodide transport in thyroid cells.
  • Analysis of functional data implicating various ion transporters in iodide (I-) movement.
  • Comparative assessment of candidate iodide (I-) transporter proteins.

Main Results:

  • Evidence suggests that Pendrin (SLC26A4) may not be the exclusive route for iodide (I-) exit from thyrocytes.
  • The Cl(-)/H(+) antiporter (CLC-5), cystic fibrosis transmembrane conductance regulator (CFTR), and sodium monocarboxylic acid transporter (SMCT1) are proposed as alternative iodide (I-) conduits.
  • These alternative transporters may play significant roles in the translocation of iodide (I-) into the intrafollicular compartment for hormone synthesis.

Conclusions:

  • The understanding of thyroid iodide (I-) transport requires revision.
  • Multiple transporters, including CLC-5, CFTR, and SMCT1, likely contribute to efficient iodide (I-) uptake and hormone synthesis.
  • Further research is needed to elucidate the precise roles and regulation of these alternative iodide (I-) transport pathways.