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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...
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...
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...
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...
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 9, 2026

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

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A possible mechanism for 2,3',4,4',5'-pentachlorobiphenyl-mediated decrease in serum thyroxine level in mice.

Yoshihisa Kato1, Mao Onishi, Koichi Haraguchi

  • 1Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University.

Biological & Pharmaceutical Bulletin
|July 24, 2013
PubMed
Summary

2,3

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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 9, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
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Published on: October 6, 2023

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:

  • Environmental toxicology
  • Endocrinology
  • Pharmacology

Background:

  • Polychlorinated biphenyls (PCBs) are persistent environmental pollutants.
  • Thyroid hormone homeostasis is crucial for mammalian development and metabolism.
  • Aryl hydrocarbon receptor (AhR) mediates toxic effects of some PCBs.

Purpose of the Study:

  • To investigate the strain-specific effects of 2,3',4,4',5'-pentachlorobiphenyl (CB118) on thyroid hormone levels in mice.
  • To elucidate the mechanisms underlying CB118-induced alterations in thyroxine (T₄) metabolism.

Main Methods:

  • Comparative study using C57BL/6 (AhR-sensitive) and DBA/2 (AhR-insensitive) mice.
  • Administration of CB118 (50 mg/kg, i.p.) for 5 days.
  • Measurement of serum total thyroxine (T₄) and thyroid-stimulating hormone (TSH) levels.
  • Assessment of hepatic T₄-uridine 5'-diphosphate (UDP)-glucuronosyltransferase (UGT) activity and expression.
  • Analysis of biliary excretion of radiolabeled T₄ and its glucuronide metabolite.
  • Evaluation of radiolabeled T₄ binding to plasma proteins (transthyretin, albumin, thyroxine-binding globulin).

Main Results:

  • CB118 significantly decreased serum total T₄ levels in both mouse strains.
  • DBA/2 mice showed decreased TSH, while C57BL/6 mice did not.
  • Hepatic T₄-UGT activity and T₄ glucuronidation increased only in CB118-treated C57BL/6 mice.
  • CB118 increased liver-selective accumulation of T₄ in both strains, suggesting enhanced hepatic uptake as a primary mechanism for T₄ reduction.

Conclusions:

  • CB118 induces hypothyroxinemia in both AhR-sensitive and insensitive mice.
  • Enhanced hepatic accumulation of thyroxine is the primary mechanism driving CB118-induced hypothyroxinemia.
  • Strain-specific differences in TSH response and hepatic UGT activity suggest complex interactions between CB118, AhR, and thyroid hormone regulation.