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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...

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...

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...

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...

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...

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Related Experiment Video

Updated: Jul 2, 2026

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

Thyroid hormones and methylmercury toxicity.

Offie P Soldin¹, Daniel M O'Mara, Michael Aschner

¹Department of Medicine, Oncology and Physiology, Center for Sex Differences, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, 3800 Reservoir Road, NW, Washington, DC 20057, USA. os35@georgetown.edu

Biological Trace Element Research

|August 22, 2008

Summary

Methylmercury (MeHg) exposure may disrupt fetal neurodevelopment by interfering with thyroid hormone balance. This occurs because mercury affects selenium, a key element for thyroid hormone activation and inactivation.

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An Anaerobic Biosensor Assay for the Detection of Mercury and Cadmium

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Last Updated: Jul 2, 2026

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

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Published on: October 6, 2023

An Anaerobic Biosensor Assay for the Detection of Mercury and Cadmium

An Anaerobic Biosensor Assay for the Detection of Mercury and Cadmium

Published on: December 17, 2018

Area of Science:

Endocrinology
Neuroscience
Toxicology

Background:

Thyroid hormones are crucial for fetal growth, development, and cellular metabolism.
Thyroid hormone homeostasis is regulated by deiodinases, enzymes dependent on selenium.
Selenium's sensitivity to mercury raises concerns about methylmercury's impact on neurodevelopment.

Purpose of the Study:

To review the potential mechanisms by which methylmercury (MeHg) may adversely affect fetal neurodevelopment.
To examine the role of thyroid hormone homeostasis disruption in MeHg-induced neurodevelopmental alterations.

Main Methods:

Literature review focusing on methylmercury, selenium, and thyroid hormone interactions.
Analysis of existing studies on the effects of organometals on deiodinase activity.
Synthesis of evidence linking altered thyroid hormone function to neurodevelopmental outcomes.

Main Results:

Methylmercury exposure can deplete selenium levels, impairing deiodinase function.
Altered thyroid hormone activation and inactivation can disrupt critical signaling pathways in the brain.
Evidence suggests a link between impaired thyroid hormone homeostasis and neurodevelopmental deficits.

Conclusions:

Methylmercury poses a risk to fetal neurodevelopment by disrupting thyroid hormone homeostasis.
Protecting selenium availability is critical for mitigating mercury's neurotoxic effects.
Further research is needed to fully elucidate the mechanisms and consequences of MeHg exposure on neurodevelopment.