Related Experiment Video
Updated: Jun 1, 2026
04:14
In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
Published on: October 6, 2023
Illness-induced changes in thyroid hormone metabolism: focus on the tissue level
J Kwakkel1, E Fliers, A Boelen
1Department of Endocrinology & Metabolism, Academic Medical Center, University of Amsterdam, the Netherlands. g.j.kwakkel@amc.uva.nl
The Netherlands Journal of Medicine
|June 8, 2011
Summary
Illness alters thyroid hormone metabolism, creating the non-thyroidal illness syndrome (NTIS). This review explores how tissue-specific changes in thyroid hormone action during NTIS impact disease progression.
Area of Science:
- Endocrinology
- Metabolic Medicine
- Physiology
Background:
- Illness triggers significant alterations in thyroid hormone metabolism, termed non-thyroidal illness syndrome (NTIS).
- NTIS is defined by reduced serum thyroid hormones despite normal or low TSH, suggesting altered feedback regulation.
- Recent research reveals tissue-specific metabolic changes in thyroid hormones during NTIS.
Purpose of the Study:
- To review systemic and local alterations in thyroid hormone metabolism during non-thyroidal illness syndrome.
- To elucidate the physiological implications of these metabolic changes on disease course.
Main Methods:
- Literature review of recent studies on thyroid hormone metabolism in illness.
- Analysis of systemic and tissue-specific changes in thyroid hormone pathways.
- Discussion of the functional consequences of altered thyroid hormone action.
Main Results:
- Non-thyroidal illness syndrome (NTIS) involves complex, tissue-dependent modifications in thyroid hormone metabolism.
- These metabolic shifts can lead to either enhanced or suppressed thyroid hormone activity at the cellular level.
- The interplay of systemic and local changes significantly influences the body's response to illness.
Conclusions:
- Understanding the differential tissue effects of NTIS is crucial for comprehending disease pathophysiology.
- Altered thyroid hormone metabolism during illness has significant physiological implications for patient outcomes.
- Further research into NTIS mechanisms can inform therapeutic strategies.
Related Concept Videos
01:27Hyperthyroidism 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...
01:23Hypothyroidism 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...
01:20Synthesis 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...
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...
01:24Graves 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...
01:25Hyperthyroidism 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...
01:28Graves' 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...