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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...
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...
Hyperthyroidism I: Introduction01:25

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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...
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...
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 novel mechanism for polychlorinated biphenyl-induced decrease in serum thyroxine level in rats.

Yoshihisa Kato1, Shin-ichi Ikushiro, Rie Takiguchi

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Drug Metabolism and Disposition: the Biological Fate of Chemicals
|July 20, 2007
PubMed
Summary

Consecutive low-dose Kanechlor-500 (KC500) treatment decreases serum thyroxine (T4) levels in rats. This reduction is linked to increased T4 accumulation in tissues, particularly the liver, not enhanced T4-UDP-GT activity.

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

  • Toxicology
  • Endocrinology
  • Pharmacology

Background:

  • Previous studies suggested Kanechlor-500 (KC500) single high-dose administration decreases serum thyroxine (T4).
  • The role of hepatic T4-UDP-glucuronosyltransferase (UDP-GT) in this decrease was unclear.
  • This study investigates the effects of consecutive low-dose KC500 exposure.

Purpose of the Study:

  • To determine if consecutive low-dose KC500 treatment decreases serum T4 levels.
  • To elucidate the exact mechanism behind KC500-induced T4 reduction.
  • To assess the involvement of hepatic T4-UDP-GT activity.

Main Methods:

  • Rats (Wistar and Gunn) received daily low-dose KC500 (10 mg/kg) for 10 days.
  • Serum T4, free T4, and thyroid-stimulating hormone levels were measured.
  • Hepatic T4-UDP-GT activity was assessed.
  • [125I]T4 clearance and tissue accumulation were evaluated.

Main Results:

  • Consecutive KC500 treatment significantly decreased serum total T4 and free T4 in both Wistar and Gunn rats.
  • Hepatic T4-UDP-GT activity increased in Wistar rats but not in Gunn rats.
  • Faster [125I]T4 clearance and increased [125I]T4 accumulation in tissues, especially the liver, were observed in KC500-treated rats.

Conclusions:

  • Consecutive low-dose KC500 exposure reduces serum T4 levels in rats.
  • The primary mechanism involves increased T4 accumulation in tissues, particularly the liver.
  • This effect is independent of significant changes in hepatic T4-UDP-GT activity.