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The Thyroid Gland

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...

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...

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...

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...

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Related Experiment Video

Updated: May 12, 2026

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

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

Published on: February 9, 2024

Selenium and the thyroid: A close-knit connection.

Ashok K Bhuyan¹, Dipti Sarma, Uma K Saikia

¹Department of Endocrinology, Gauhati Medical College, India.

Indian Journal of Endocrinology and Metabolism

|April 9, 2013

Summary

This summary is machine-generated.

Selenium supplementation significantly reduced thyroid inflammation markers in patients with autoimmune thyroid disease. Further research is needed to explore selenium

Keywords:

Selenium thyroid

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

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Published on: October 6, 2023

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Last Updated: May 12, 2026

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

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

Published on: February 9, 2024

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

Area of Science:

Endocrinology
Immunology
Nutritional Science

Background:

Severe selenium deficiency is linked to increased thyroiditis incidence.
Reduced activity of selenium-dependent glutathione peroxidase in thyroid cells contributes to thyroiditis.

Purpose of the Study:

To investigate the therapeutic effect of selenium supplementation in patients diagnosed with autoimmune thyroid disease.

Main Methods:

A blinded, placebo-controlled prospective study involved 60 patients with autoimmune thyroid disease (anti-thyroid peroxidase antibody > 150 IU/ml).
Patients received either 200 μg/day of sodium selenite or a placebo for 3 months.
Exclusion criteria included overt hyperthyroidism, medications affecting immunity, and pregnancy. Hypothyroid patients received l-thyroxine replacement.

Main Results:

The selenium group showed a significant 49.5% decrease in mean anti-thyroid peroxidase antibody (TPOAb) levels (P < 0.013).
The placebo group experienced only a 10.1% decrease in TPOAb levels (P < 0.95).

Conclusions:

Selenium substitution demonstrates a notable impact on inflammatory activity in autoimmune thyroid diseases.
Investigating early selenium treatment could reveal potential to delay or prevent autoimmune thyroiditis progression.