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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...
Functions of Thyroid Hormones01:18

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...
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...
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...

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Updated: May 30, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Thyroid hormone transport in developing brain.

Juan Bernal1

  • 1Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain. jbernal@iib.uam.es

Current Opinion in Endocrinology, Diabetes, and Obesity
|August 10, 2011
PubMed
Summary
This summary is machine-generated.

Recent advances in thyroid hormone transport reveal the critical role of the MCT8 gene in brain development. Mutations cause Allan-Herndon-Dudley syndrome, leading to myelination delays and neurological issues.

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Area of Science:

  • Neuroendocrinology
  • Molecular Genetics
  • Developmental Neuroscience

Background:

  • Thyroid hormones are crucial for brain development and function.
  • Thyroid hormone transport across cell membranes is mediated by specific transporters, notably MCT8.
  • Defects in thyroid hormone transport can lead to severe neurological disorders.

Purpose of the Study:

  • To review recent advancements in understanding thyroid hormone transport in the brain.
  • To highlight the specific role of the MCT8 gene and its mutations in the X-linked thyroid hormone cell transport (THCT) defect, also known as Allan-Herndon-Dudley syndrome.

Main Methods:

  • Review of current literature on MCT8 function and THCT defect.
  • Analysis of neuroimaging (MRI) findings in patients with THCT defect.
  • Examination of molecular mechanisms involving MCT8, deiodinases, and thyroid hormone metabolism.

Main Results:

  • MCT8 is essential for thyroid hormone transport in the brain, impacting oligodendrocyte function and myelination.
  • MRI studies in THCT defect patients show myelination delays.
  • MCT8 also plays a role in thyroid hormone secretion, with altered peripheral metabolism and increased deiodinase activity contributing to the syndrome's pathophysiology.
  • Elevated D1 activity in the liver and kidney increases serum T3, while enhanced brain D2 activity attempts to compensate for deficient T3 transport.

Conclusions:

  • Screening for MCT8 gene mutations is recommended for patients with suspected X-linked leukoencephalopathy.
  • Further research should investigate the specific role of MCT8 in oligodendrocyte function and myelination to understand the brain pathophysiology of THCT defect.