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Related Concept Videos

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 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...
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...
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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
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...

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Related Experiment Video

Updated: Jun 13, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
04:14

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

Published on: October 6, 2023

[Disorders in thyroid hormone metabolism].

Yasumasa Iwasaki1

  • 1Department of Endocrinology, Metabolism, and Nephrology, Health Care Center, Kochi University, Kochi 780-8520, Japan. iwasaki@kochi-u.ac.jp

Rinsho Byori. the Japanese Journal of Clinical Pathology
|April 23, 2010
PubMed
Summary
This summary is machine-generated.

Serum thyroid hormone levels depend on synthesis and metabolism. Three selenodeiodinases (D1, D2, D3) regulate this metabolism, influencing thyroid hormone availability and function.

Related Experiment Videos

Last Updated: Jun 13, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
04:14

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

Published on: October 6, 2023

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Serum thyroid hormone levels (free T4, free T3) are influenced by synthesis, secretion, and metabolism.
  • Thyroid hormone metabolism is primarily mediated by three key selenoproteins: selenodeiodinase type 1, 2, and 3 (D1, D2, D3).
  • These enzymes exhibit tissue-specific regulation, impacting intracellular thyroid hormone availability.

Purpose of the Study:

  • To elucidate the roles of D1, D2, and D3 in thyroid hormone metabolism.
  • To understand the regulatory mechanisms governing these selenoproteins.
  • To explore genetic factors and external influences on thyroid hormone homeostasis.

Main Methods:

  • Analysis of selenoprotein expression and function.
  • Investigation of tissue-specific regulation of deiodinases.
  • Review of genetic mutations and environmental factors affecting thyroid hormone metabolism.

Main Results:

  • D2 enhances intracellular thyroid hormone levels, while D3 decreases them.
  • D1 functions as a general housekeeping or scavenger enzyme in thyroid hormone metabolism.
  • While deiodinase genes themselves show no reported mutations, mutations in related genes (SECISBP2, DEHAL1, MCT8) can lead to inherited thyroid disorders.
  • Hormones, cytokines, and drugs can modulate thyroid function by altering thyroid hormone metabolism.

Conclusions:

  • Selenodeiodinases are critical regulators of thyroid hormone homeostasis.
  • Dysregulation of these enzymes or related genetic factors can result in thyroid dysfunction.
  • Understanding these metabolic pathways is crucial for diagnosing and managing thyroid-related disorders.