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Hyperthyroidism I: Introduction

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...

Hyperthyroidism II: Pathophysiology

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: Pathophysiology

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...

Graves Disease II: Pathophysiology

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...

Graves' Disease I: Introduction

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...

Synthesis and Regulation of Thyroid Hormones

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...

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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

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Oxidative stress in cold-induced hyperthyroid state.

P Venditti¹, L Di Stefano, S Di Meo

¹Department of the Biological Sciences, Section of Physiology, University Federico II of Naples, 80134, Naples, Italy. venditti@unina.it

The Journal of Experimental Biology

|August 17, 2010

Summary

This summary is machine-generated.

Cold exposure causes oxidative stress in animals, potentially due to thyroid hormone triiodothyronine (T3). This hormone plays a key role in the thermogenic response and tissue damage during cold conditions.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Area of Science:

Physiology
Endocrinology
Biochemistry

Background:

Low environmental temperature exposure induces oxidative stress in homeothermic animals.
Cold exposure leads to a state of functional hyperthyroidism.
Tissue oxidative stress is also observed in experimental hyperthyroidism induced by triiodothyronine (T3) treatment.

Purpose of the Study:

To investigate the role of thyroid hormone triiodothyronine (T3) in mediating oxidative stress during cold exposure.
To compare oxidative stress mechanisms in functional hyperthyroidism (cold-exposed) and experimental hyperthyroidism (T3-treated).

Main Methods:

Comparative analysis of oxidative stress markers in T3-responsive tissues (brown adipose tissue and liver) from cold-exposed and T3-treated animals.
Examination of the interplay between T3, noradrenaline, and thyroxine in cold-induced oxidative damage.

Main Results:

Similar changes in factors favoring oxidative modifications were observed in both experimental and functional hyperthyroidism.
Differences in oxidative stress were noted, attributed to varying levels of physiological regulators like noradrenaline and thyroxine.
Evidence suggests a synergistic action between T3 and noradrenaline signals in thermogenesis and oxidative stress during cold exposure.
Thyroxine (T4) directly contributes to oxidative damage in brown adipose tissue (BAT) during cold exposure but acts as a T3 precursor in the liver.

Conclusions:

Triiodothyronine (T3) is a key mediator of oxidative stress in animals exposed to cold.
Noradrenaline and T3 signaling synergize to drive both thermogenesis and oxidative damage.
Thyroxine (T4) has distinct roles in different tissues, directly impacting BAT oxidative stress while serving as a T3 precursor in the liver.