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Related Concept Videos

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...
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 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...
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: May 20, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Increased type 3 deiodinase expression in papillary thyroid carcinoma.

Mírian Romitti1, Simone Magagnin Wajner, Nadja Zennig

  • 1Thyroid Section, Endocrine Division, Hospital de Clinicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2350, Porto Alegre, RS, Brazil.

Thyroid : Official Journal of the American Thyroid Association
|July 25, 2012
PubMed
Summary

Papillary thyroid carcinoma (PTC) reactivates the thyroid-hormone-inactivating type 3 deiodinase (DIO3), increasing its activity and mRNA levels. This enhanced DIO3 expression correlates with advanced disease, suggesting a role in tumor progression.

Related Experiment Videos

Last Updated: May 20, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid hormone is crucial for cellular functions, including proliferation and differentiation.
  • The type 3 deiodinase (DIO3), which inactivates thyroid hormone, is reactivated in human cancers.
  • This study investigates DIO3 expression in human papillary thyroid carcinoma (PTC).

Purpose of the Study:

  • To evaluate DIO3 expression and activity in human PTC.
  • To explore the regulatory mechanisms of DIO3 in PTC.
  • To correlate DIO3 levels with clinical parameters and disease progression.

Main Methods:

  • Analysis of DIO3 mRNA and activity in PTC tissues and cell lines.
  • Investigation of DIO3 gene regulation by TGFβ1 and MAPK signaling pathway.
  • Detection of BRAF(V600E) mutation and immunohistochemistry for D3.
  • Retrospective review of clinical data from 26 PTC patients.

Main Results:

  • All PTC samples showed increased DIO3 activity and mRNA levels compared to normal tissue.
  • DIO3 expression was upregulated by TGFβ1 via the MAPK pathway.
  • Higher DIO3 levels were observed in BRAF(V600E)-mutated PTC and correlated with tumor size and metastasis.
  • Decreased DIO2 (thyroid-hormone-activating) expression was noted in PTC.

Conclusions:

  • Malignant transformation to PTC alters DIO3 and DIO2 expression via pretranscriptional mechanisms.
  • Increased DIO3 activity is associated with advanced PTC, suggesting a role in tumor cell proliferation and dedifferentiation.
  • DIO3 is also upregulated in follicular thyroid carcinoma but not in medullary or anaplastic types.