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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...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
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 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...
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...
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...

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Related Experiment Video

Updated: Jul 20, 2026

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
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Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

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Selenium supplementation for autoimmune thyroiditis: a systematic review and meta-analysis.

Yaofu Fan1, Shuhang Xu1, Huifeng Zhang1

  • 1Endocrine and Diabetes Center, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210000, China.

International Journal of Endocrinology
|January 10, 2015
PubMed
Summary

Selenium supplementation may benefit autoimmune thyroiditis (AIT) by reducing thyroid antibodies like TPOAb and TgAb over time. Patients may also experience improved mood and well-being without significant adverse effects.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Area of Science:

  • Endocrinology
  • Immunology
  • Nutritional Science

Background:

  • Autoimmune thyroiditis (AIT) is linked to selenium (Se) levels.
  • The therapeutic role of Se supplementation in AIT is not fully understood.

Purpose of the Study:

  • To evaluate the efficacy of Se supplementation in treating AIT.
  • To analyze the impact of Se on thyroid antibody titers and patient well-being.

Main Methods:

  • Systematic literature search for randomized controlled trials.
  • Inclusion of nine studies with a total of 787 AIT patients.
  • Comparison of Se supplementation versus placebo groups.

Main Results:

  • Se supplementation for 6 months significantly reduced TPOAb titers.
  • Se supplementation for 12 months significantly reduced both TPOAb and TgAb titers.
  • Patients receiving Se showed improved mood and well-being with no significant adverse events.

Conclusions:

  • Se supplementation effectively decreases TPOAb at 6 and 12 months and TgAb at 12 months.
  • Selenium may improve mood in AIT patients without notable side effects.
  • Further research may clarify optimal Se dosage and duration for AIT management.