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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

58
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...
58
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

58
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...
58
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

59
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,...
59
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

64
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...
64
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

7.2K
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...
7.2K
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

52
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...
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Pregnancy negates thyroid hormone-induced pyrexia.

Nuria López-Alcántara1,2, Lena Adam1,2, Julia Resch2

  • 1Institute for Experimental Endocrinology-Group Thyroid and BAT Programming, Center of Brain Behavior and Metabolism (CBBM), University of Luebeck/UKSH, Luebeck, Germany.

American Journal of Physiology. Endocrinology and Metabolism
|May 6, 2026
PubMed
Summary
This summary is machine-generated.

Maternal thyroid hormone (TH) influences pregnancy thermoregulation. This study shows TH protects the fetus from overheating by adjusting maternal metabolism and endocrine signals, ensuring fetal viability and maternal energy balance.

Keywords:
brown adipose tissuebrowningfibroblast growth factor 21pregnancythyroid hormone

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Area of Science:

  • Reproductive biology
  • Endocrinology
  • Physiology

Background:

  • Thyroid hormone (TH) regulates body temperature.
  • The role of TH in maternal thermoregulation during pregnancy is unknown.
  • Maintaining fetal viability requires precise control of maternal physiology.

Purpose of the Study:

  • To investigate the effects of maternal hyperthyroidism on thermoregulation, metabolic tissues, and endocrine signaling in pregnant mice.
  • To understand how thyroid hormone impacts maternal-fetal energy balance and fetal development.

Main Methods:

  • Pregnant mice were treated with 3,3',5-Triiodo-L-thyronine (T3) from conception to late gestation.
  • Core body temperature, thermogenic activation in adipose tissues, and skeletal muscle metabolism were assessed.
  • Endocrine signaling, including FGF21, was analyzed.

Main Results:

  • Maternal T3 initially elevated core temperature but attenuated towards term, allowing normal prepartum temperature drop.
  • Adipose tissues showed no thermogenic activation despite elevated TH.
  • Skeletal muscle underwent metabolic remodeling, and FGF21 levels increased, supporting maternal metabolic demands.

Conclusions:

  • Pregnancy involves a unique mechanism where central TH effects are modulated to prevent fetal hyperthermia.
  • Peripheral thermogenic activation is suppressed, and endocrine signaling is redirected to maintain maternal-fetal energy balance.
  • Findings have implications for thyroid dysfunction during pregnancy and fetal programming.