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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...
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...
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...

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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 2,2',4,4',5,5'-hexachlorobiphenyl-mediated decrease in serum thyroxine level in mice.

Yoshihisa Kato1, Mao Onishi, Koichi Haraguchi

  • 1Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Sanuki, Kagawa, Japan. kato@kph.bunri-u.ac.jp

Toxicology and Applied Pharmacology
|May 17, 2011
PubMed
Summary

Hexachlorobiphenyl (CB153) exposure significantly reduced serum thyroxine (T₄) levels in mice. This decrease was primarily due to increased T₄ accumulation in the liver, not altered metabolism or protein binding.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Area of Science:

  • Environmental Toxicology
  • Endocrinology

Background:

  • Polychlorinated biphenyls (PCBs) are environmental contaminants with known endocrine-disrupting effects.
  • Thyroxine (T₄) is a critical thyroid hormone regulating metabolism.
  • Understanding PCB-induced alterations in thyroid hormone homeostasis is crucial for risk assessment.

Purpose of the Study:

  • To investigate the impact of 2,2',4,4',5,5'-hexachlorobiphenyl (CB153) on serum total thyroxine (T₄) levels in mice.
  • To elucidate the mechanisms underlying CB153-induced changes in T₄ homeostasis, including hepatic metabolism and serum protein binding.

Main Methods:

  • Administration of CB153 (100mg/kg, ip) to C57BL/6 (TCDD-sensitive) and DBA/2 (TCDD-resistant) mice.
  • Measurement of serum total T₄, hepatic T₄-UDP-glucuronosyltransferase (T₄-UGT), and serum thyroid-stimulating hormone (TSH) levels.
  • Assessment of [(125)I]T₄ binding to serum proteins and analysis of biliary excretion of [(125)I]T₄ and its glucuronide.

Main Results:

  • CB153 treatment markedly decreased serum total T₄ levels in both mouse strains without affecting hepatic T₄-UGT or serum TSH.
  • No significant changes in [(125)I]T₄ binding to serum transport proteins were observed.
  • CB153 exposure led to increased hepatic accumulation of [(125)I]T₄ in both strains, with higher percentages observed in C57BL/6 mice.

Conclusions:

  • CB153 exposure induces a significant reduction in serum total T₄ levels in mice.
  • The primary mechanism for this T₄ reduction is enhanced hepatic accumulation of T₄, rather than altered T₄ metabolism or serum binding.
  • These findings highlight the liver as a key target organ for CB153's effects on thyroid hormone homeostasis.