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Related Concept Videos

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...
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...
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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Related Experiment Video

Updated: May 22, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Transcriptome-level microarray expression profiling implicates IGF-1 and Wnt signalling dysregulation in the

Daniel G Ezra1, Jonathan Krell, Geoffrey E Rose

  • 1NIHR Biomedical Research Centre for Ophthalmology, Moorfields Eye Hospital, London, UK. d.ezra@ucl.ac.uk

Journal of Clinical Pathology
|May 5, 2012
PubMed
Summary

Thyroid-associated orbitopathy (TAO) pathogenesis involves altered Insulin-like Growth Factor-1 (IGF-1) and Wnt signaling pathways. This study reveals IGF-1 pathway gene dysregulation in TAO orbital fat, suggesting its role in disease development and treatment.

Related Experiment Videos

Last Updated: May 22, 2026

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:

  • Endocrinology
  • Molecular Biology
  • Ophthalmology

Background:

  • Thyroid-associated orbitopathy (TAO) pathogenesis is not fully understood.
  • Orbital fat gene expression in active, untreated TAO requires elucidation.

Purpose of the Study:

  • To investigate the gene expression profile of orbital fat in patients with active, untreated TAO.
  • To identify key molecular pathways involved in TAO pathogenesis.

Main Methods:

  • Case-control gene expression study using orbital fat specimens from TAO patients and controls.
  • cDNA expression analysis via Affymetrix GeneChip Human Genome U133 Plus 2.0 platform.
  • Validation of findings using quantitative PCR.

Main Results:

  • Insulin-like Growth Factor-1 (IGF-1) signaling genes were significantly differentially expressed, including IGF-1, IGF-1 receptor, SOCS3, IRS2, SGK, and c-JUN.
  • Dysregulation of wingless-type MMTV (Wnt) signaling pathway genes (Wnt5a, sFRPs, DKK) was observed.
  • Microarray data indicated significant alterations in IGF-1 and Wnt signaling pathways.

Conclusions:

  • Altered Wnt signaling in TAO orbital fat is confirmed.
  • The study provides the first evidence of IGF-1 pathway gene dysregulation in TAO tissue.
  • IGF-1 signaling is implicated in TAO pathogenesis and may represent a therapeutic target.