Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

Thyrotropin-Releasing Hormone (TRH) and Somatostatin (SST), but not Growth Hormone-Releasing Hormone (GHRH) nor Ghrelin (GHRL), Regulate Expression and Release of Immune Growth Hormone (GH) from Chicken Bursal B-Lymphocyte Cultures

Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

Open AccessArticle

bySantiago Pech-Pool 1,2, Laura C. Berumen 2, Carlos G. Martínez-Moreno 1, Guadalupe García-Alcocer 2, Martha Carranza 1, Maricela Luna 1,3,* and Carlos Arámburo 1,3,*

1

Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Campus Juriquilla, Universidad Nacional Autónoma de México, Querétaro 76230, Mexico

2

Posgrado en Ciencias Químico-Biológicas, Facultad de Química, Universidad Autónoma de Querétaro, Centro Universitario, Querétaro 76010, Mexico

3

Instituto de Neurobiología, Universidad Nacional Autónoma de México, Boulevard Juriquilla 3001, Querétaro 76230, Mexico

*

Authors to whom correspondence should be addressed.

Int. J. Mol. Sci. 2020, 21(4), 1436; https://doi.org/10.3390/ijms21041436

Received: 30 January 2020 / Revised: 14 February 2020 / Accepted: 16 February 2020 / Published: 20 February 2020

View Full-TextDownload PDF It is known that growth hormone (GH) is expressed in immune cells, where it exerts immunomodulatory effects. However, the mechanisms of expression and release of GH in the immune system remain unclear. We analyzed the effect of growth hormone-releasing hormone (GHRH), thyrotropin-releasing hormone (TRH), ghrelin (GHRL), and somatostatin (SST) upon GH mRNA expression, intracellular and released GH, Ser133-phosphorylation of CREB (pCREBS133), intracellular Ca2+ levels, as well as B-cell activating factor (BAFF) mRNA expression in bursal B-lymphocytes (BBLs) cell cultures since several GH secretagogues, as well as their corresponding receptors (-R), are expressed in B-lymphocytes of several species. The expression of TRH/TRH-R, ghrelin/GHS-R1a, and SST/SST-Rs (Subtypes 1 to 5) was observed in BBLs by RT-PCR and immunocytochemistry (ICC), whereas GHRH/GHRH-R were absent in these cells. We found that TRH treatment significantly increased local GH mRNA expression and CREB phosphorylation. Conversely, SST decreased GH mRNA expression. Additionally, when added together, SST prevented TRH-induced GH mRNA expression, but no changes were observed in pCREBS133 levels. Furthermore, TRH stimulated GH release to the culture media, while SST increased the intracellular content of this hormone. Interestingly, SST inhibited TRH-induced GH release in a dose-dependent manner. The coaddition of TRH and SST decreased the intracellular content of GH. After 10 min. of incubation with either TRH or SST, the intracellular calcium levels significantly decreased, but they were increased at 60 min. However, the combined treatment with both peptides maintained the Ca2+ levels reduced up to 60-min. of incubation. On the other hand, BAFF cytokine mRNA expression was significantly increased by TRH administration. Altogether, our results suggest that TRH and SST are implicated in the regulation of GH expression and release in BBL cultures, which also involve changes in pCREBS133 and intracellular Ca2+ concentration. It is ly that TRH, SST, and GH exert autocrine/paracrine immunomodulatory actions and participate in the maturation of chicken BBLs.View Full-Text

Keywords: bursa of fabricius; growth hormone; bursal B-lymphocytes; TRH; somatostatin; GHRH bursa of fabricius; growth hormone; bursal B-lymphocytes; TRH; somatostatin; GHRH

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MDPI and ACS Style

Pech-Pool, S.; Berumen, L.C.; Martínez-Moreno, C.G.; García-Alcocer, G.; Carranza, M.; Luna, M.; Arámburo, C. Thyrotropin-Releasing Hormone (TRH) and Somatostatin (SST), but not Growth Hormone-Releasing Hormone (GHRH) nor Ghrelin (GHRL), Regulate Expression and Release of Immune Growth Hormone (GH) from Chicken Bursal B-Lymphocyte Cultures. Int. J. Mol. Sci. 2020, 21, 1436.

AMA Style

Pech-Pool S, Berumen LC, Martínez-Moreno CG, García-Alcocer G, Carranza M, Luna M, Arámburo C. Thyrotropin-Releasing Hormone (TRH) and Somatostatin (SST), but not Growth Hormone-Releasing Hormone (GHRH) nor Ghrelin (GHRL), Regulate Expression and Release of Immune Growth Hormone (GH) from Chicken Bursal B-Lymphocyte Cultures. International Journal of Molecular Sciences. 2020; 21(4):1436.

Chicago/Turabian Style

Pech-Pool, Santiago; Berumen, Laura C.; Martínez-Moreno, Carlos G.; García-Alcocer, Guadalupe; Carranza, Martha; Luna, Maricela; Arámburo, Carlos. 2020.

“Thyrotropin-Releasing Hormone (TRH) and Somatostatin (SST), but not Growth Hormone-Releasing Hormone (GHRH) nor Ghrelin (GHRL), Regulate Expression and Release of Immune Growth Hormone (GH) from Chicken Bursal B-Lymphocyte Cultures.” Int. J. Mol. Sci. 21, no. 4: 1436.

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Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

Thyrotropin-releasing hormone (TRH) is a hormone produced in the hypothalamus. It controls thyroid hormone secretion and has important roles in metabolism, cognition, mental health, and more. This post reveals lesser-known roles of TRH, along with 13 factors that increase or decrease its levels.

What is Thyrotropin-Releasing Hormone (TRH)?

Thyrotropin-releasing hormone (TRH) is a hormone produced in the hypothalamus. It stimulates the release of TSH, which then increases thyroid hormones. Thus, TRH controls [1]:

  • energy balance (homeostasis)
  • eating patterns
  • thermogenesis (heat production)
  • autonomic regulation (the unconscious control of vital bodily functions)

The hypothalamus, pituitary, and the thyroid gland (also called the hypothalamic-pituitary-thyroid or HPT axis) controls T4 levels [2].

These three glands release the following hormones: TRH (Hypothalamus) -> TSH (Pituitary) -> T4 (Thyroid).

If there is too little of the thyroid hormones in the bloodstream, the hypothalamus will signal the pituitary gland (via TRH) to produce TSH for the thyroid to release more T4.

Hypothyroidism that is caused by low TRH is called hypothalamic hypothyroidism, or central hypothyroidism.

Reference Range

Normal Range of TRH is 5-25 U/ml, but it may depend on the lab.

1) Learning and Memory

TRH is widely found in the brains of mammals and is considered a neurotransmitter [3].

Whether TRH has a positive or neutral effect on cognitive function is still debated.

A rat model of Alzheimer’s showed no beneficial effects of TRH in learning and memory [4].

However, other studies have found TRH to enhance learning and reduce memory impairment [3].

In rabbits, chronically high levels of TRH improved learning and memory [3].

TRH and similar hormones are promising research agents in the treatment of brain degeneration, but the clinical evidence is lacking [1].

2) Mental Health

Depressed patients do not produce as much TSH in response to TRH and have decreased TRH gene expression in the hypothalamus. Hypothyroidism is found in many patients with major depression [5, 6].

In mice, TRH functions by activating two receptors – TRH-R1 and TRH-R2, the latter of which is not found in humans. Activation of these receptors initiates a number of effects in the brain. Mice lacking TRH receptor type 1 (TRH-R1) are more depressed and anxious. These mice exhibited hypothyroidism [7].

Mice lacking TRH receptor type 2 (TRH-R2) have no thyroid abnormalities, with regular development and growth. However, female mice were slightly more depressed but less anxious than male mice [7].

Rats treated with TRH showed less anxiety in stressful situations [8].

3) Appetite Control

TRH may suppress appetite. Both fed and food-restricted animals ate less food when injected with TRH [9].

Generally, the presence of healthy dopamine levels can reduce eating for pleasure, which helps with weight loss. Hungry rats injected with TRH had more dopamine [10, 9].

4) Blood Sugar Control

TRH is also made in the pancreas. It inhibits amylase secretion and increases glucagon secretion from the pancreas [11].

Genetically modified mice that lack TRH have elevated blood sugar (hyperglycemia) [12].

Injection of TRH combats elevated blood sugar in hyperglycemic mice, by reducing damage and stimulating regeneration of insulin-producing cells in the pancreas [12].

5) Digestion

In the brain, TRH acts through the vagus nerve to increase stomach acid, pepsin, and serotonin, blood flow in the gut lining, and contraction [13, 14].

6) Prolactin Secretion

The secretion of TRH can also stimulate the release of prolactin, another hormone from the pituitary gland [15].

1) Low Thyroid Hormones

If there is too little of the thyroid hormones in the bloodstream, the hypothalamus will signal the pituitary gland (via TRH) to produce TSH for the thyroid to release more T3 and T4 [16].

Once there is enough of these hormones, they signal the hypothalamus and pituitary to stop this cascade of actions and drop T3 and T4 levels.

2) Estrogen (Estradiol)

E2 decreases the effects of ghrelin on the hypothalamus, which also reduces the activity of agouti and neuropeptide Y. This increases levels of TRH in rats [17].

In menopausal mice, feeding estrogen (E2) increased TRH and thyroid hormone levels [18].

3) Cold Exposure

Cold exposure increases TRH, according to preclinical research. In rats, exposure to 4 degrees C or 39 degrees F increased TRH release by twofold in the first 15 minutes [19, 20, 21, 22].

4) Drugs

Lithium increases the TRH production and the response of TSH to TRH [23, 24].

Valproate and lithium increase levels of TRH receptors in the brain [25].

In rats, administration of ketamine (anesthetic) increases TRH levels in most regions of the brain and the body [26].

5) Other

Inhibiting Sirt1

In diet-induced obese rats, inhibiting Sirt1 increased TRH level. Read this post to learn about the factors that inhibit Sirt1.

This effect is possibly mediated through circadian rhythm, by changing POMC and a-MSH levels [27].

Electroconvulsive Therapy

Electroconvulsive therapy is a treatment for treatment-resistant depression. In rats, electroconvulsive therapy increased TRH levels, which correlated well with the reduction in depressive symptoms [28].

1) High Thyroid Hormones

High Free T4 and Free T3 levels can signal the pituitary and hypothalamus to adjust TSH and TRH levels.

T4 increases the production of pyroglutamyl peptidase II, an enzyme that degrades TRH in the hypothalamus [29].

2) Stress and High Cortisol

Cortisol can inhibit the HPT axis by reducing TRH levels at the hypothalamus [30, 31].

However, in cell-based experiments, cortisol stimulated TRH production [31].

3) Inflammation

In rats, injection of LPS (a bacterial toxin) suppresses the production of TRH, TSH, and T3 levels, while increasing CRH and cortisol levels [32].

A high dose of LPS injection in rats reduced TRH levels within 2 hours [33].

Chronic inflammation in mice reduces TRH production in mice and rabbits [34, 35].

Injection of IL-1, TNF, and IFN-gamma either in the blood or the brain results in a fall of plasma TSH levels in rats. This may be because TNF reduces TRH production in rat hypothalamus [36, 37, 38].

4) Orexin

Injection of orexin-A in rats inhibits TRH release from the hypothalamus, leading to a reduction in TSH levels but no change in thyroid hormone levels [39].

5) Adipokine Signaling

NPY suppresses TRH production [40].

Ghrelin blocks GABA release from Agouti or NPY neurons of the hypothalamus, which decreases TRH levels [41].

6) Leptin Resistance

Leptin-resistant humans have signs of hypothalamic hypothyroidism (hypothyroidism due to how TRH) with low T4 and normal TSH [42].

A leptin analog increased FT3 and FT4 in leptin-deficient children, and reversed low T3 and T4 levels in people on a low-calorie diet [42, 43].

High leptin levels in newborn rats can lead to leptin resistance and low TRH at 30 days of age and at adulthood. In these animals, acute cold exposure at 30 days old restores normal leptin levels and leptin sensitivity in the hypothalamus. Additionally, cold exposure further increased thyroid hormones [44].

In rats, the administration of a high dose of leptin reduces TRH levels within 30 minutes by causing leptin resistance [45].

7) Fasting and Starvation

Fasting reduces leptin levels, TRH & TSH production, and liver enzymes that convert T4 to T3 [46].

However, leptin administration does not reverse changes in thyroid hormone levels in acute fasting [47].

8) Chemotherapy

Some acute lymphoblastic leukemia patients treated with chemotherapy alone may develop central hypothyroidism, which can be treated with TRH infusion [48].

Source: https://selfhacked.com/blog/trh-hpt-axis-increase-decrease/

What is the role of thyrotropin-releasing hormone (TRH) in the pathogenesis of hyperthyroidism?

Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

  1. Blick C, Jialal I. Thyroid, Thyrotoxicosis. 2018 Jan. [Medline]. [Full Text].

  2. Frost L, Vestergaard P, Mosekilde L. Hyperthyroidism and risk of atrial fibrillation or flutter: a population-based study. Arch Intern Med. 2004 Aug 9-23. 164(15):1675-8. [Medline].

  3. [Guideline] Bahn Chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. 2011 Jun. 21(6):593-646. [Medline].

  4. [Guideline] Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016 Oct. 26 (10):1343-1421. [Medline]. [Full Text].

  5. Gupta MK. Thyrotropin-receptor antibodies in thyroid diseases: advances in detection techniques and clinical applications. Clin Chim Acta. 2000 Mar. 293 (1-2):1-29. [Medline].

  6. Feldt-Rasmussen U, Hoier-Madsen M, Bech K, et al. Anti-thyroid peroxidase antibodies in thyroid disorders and non-thyroid autoimmune diseases. Autoimmunity. 1991. 9 (3):245-54. [Medline].

  7. Lumbroso S, Paris F, Sultan C. Activating Gsalpha mutations: analysis of 113 patients with signs of McCune-Albright syndrome–a European Collaborative Study. J Clin Endocrinol Metab. 2004 May. 89(5):2107-13. [Medline].

  8. Betterle C, Dal Pra C, Mantero F, Zanchetta R. Autoimmune adrenal insufficiency and autoimmune polyendocrine syndromes: autoantibodies, autoantigens, and their applicability in diagnosis and disease prediction. Endocr Rev. 2002 Jun. 23(3):327-64. [Medline].

  9. Plagnol V, Howson JM, Smyth DJ, Walker N, Hafler JP, Wallace C, et al. Genome-wide association analysis of autoantibody positivity in type 1 diabetes cases. PLoS Genet. 2011 Aug. 7(8):e1002216. [Medline]. [Full Text].

  10. Chu X, Pan CM, Zhao SX, Liang J, Gao GQ, Zhang XM, et al. A genome-wide association study identifies two new risk loci for Graves' disease. Nat Genet. 2011 Aug 14. 43(9):897-901. [Medline].

  11. Simmonds MJ, Brand OJ, Barrett JC, Newby PR, Franklyn JA, Gough SC. Association of Fc receptor- 5 (FCRL5) with Graves' disease is secondary to the effect of FCRL3. Clin Endocrinol (Oxf). 2010 Nov. 73(5):654-60. [Medline]. [Full Text].

  12. Newby PR, Pickles OJ, Mazumdar S, Brand OJ, Carr-Smith JD, Pearce SH, et al. Follow-up of potential novel Graves' disease susceptibility loci, identified in the UK WTCCC genome-wide nonsynonymous SNP study. Eur J Hum Genet. 2010 Sep. 18(9):1021-6. [Medline]. [Full Text].

  13. Nakabayashi K, Shirasawa S. Recent advances in the association studies of autoimmune thyroid disease and the functional characterization of AITD-related transcription factor ZFAT. Nihon Rinsho Meneki Gakkai Kaishi. 2010. 33(2):66-72. [Medline].

  14. Chu X, Dong Y, Shen M, Sun L, Dong C, Wang Y, et al. Polymorphisms in the ADRB2 gene and Graves disease: a case-control study and a meta-analysis of available evidence. BMC Med Genet. 2009 Mar 13. 10:26. [Medline]. [Full Text].

  15. Gabriel EM, Bergert ER, Grant CS, van Heerden JA, Thompson GB, Morris JC. Germline polymorphism of codon 727 of human thyroid-stimulating hormone receptor is associated with toxic multinodular goiter. J Clin Endocrinol Metab. 1999 Sep. 84(9):3328-35. [Medline].

  16. van Dijk MM, Smits IH, Fliers E, Bisschop PH. Maternal Thyrotropin Receptor Antibody Concentration and the Risk of Fetal and Neonatal Thyrotoxicosis: A Systematic Review. Thyroid. 2018 Feb. 28 (2):257-64. [Medline].

  17. Mittra ES, Niederkohr RD, Rodriguez C, El-Maghraby T, McDougall IR. Uncommon causes of thyrotoxicosis. J Nucl Med. 2008 Feb. 49(2):265-78. [Medline].

  18. Davies TF, Larsen PR. Thyrotoxicosis. Larsen PR et al, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia: Saunders; 2003. 374-421.

  19. White A, Bozso SJ, Moon MC. Thyrotoxicosis induced cardiomyopathy requiring support with extracorporeal membrane oxygenation. J Crit Care. 2018 Feb 3. 45:140-3. [Medline].

  20. Dahl P, Danzi S, Klein I. Thyrotoxic cardiac disease. Curr Heart Fail Rep. 2008 Sep. 5(3):170-6. [Medline].

  21. Zhyzhneuskaya S, Addison C, Tsatlidis V, Weaver JU, Razvi S. The Natural History of Subclinical Hyperthyroidism in Graves' Disease: The Rule of Thirds. Thyroid. 2016 Jun. 26(6):765-9. [Medline].

  22. Heeringa J, Hoogendoorn EH, van der Deure WM, et al. High-normal thyroid function and risk of atrial fibrillation: the Rotterdam study. Arch Intern Med. 2008 Nov 10. 168(20):2219-24. [Medline].

  23. Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab. 2002 Feb. 87(2):489-99. [Medline]. [Full Text].

  24. Porterfield JR Jr, Thompson GB, Farley DR, Grant CS, Richards ML. Evidence-based management of toxic multinodular goiter (Plummer's Disease). World J Surg. 2008 Jul. 32(7):1278-84. [Medline].

  25. [Guideline] De Groot L, Abalovich M, Alexander EK, Amino N, Barbour L, Cobin RH, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012 Aug. 97(8):2543-65. [Medline].

  26. FDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). US Food and Drug Administration. Accessed: June 3, 2009. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm.

  27. Stalberg P, Svensson A, Hessman O, et al. Surgical treatment of Graves' disease: evidence-based approach. World J Surg. 2008 Jul. 32(7):1269-77. [Medline].

  28. Wang J, Qin L. Radioiodine therapy versus antithyroid drugs in Graves' disease: a meta-analysis of randomized controlled trials. Br J Radiol. 2016 Jun 27. [Medline].

  29. Sisson JC, Freitas J, McDougall IR, Dauer LT, Hurley JR, Brierley JD, et al. Radiation safety in the treatment of patients with thyroid diseases by radioiodine ¹³¹i: practice recommendations of the american thyroid association. Thyroid. 2011 Apr. 21(4):335-46. [Medline].

  30. Shindo M. Surgery for hyperthyroidism. ORL J Otorhinolaryngol Relat Spec. 2008. 70(5):298-304. [Medline].

  31. Worni M, Schudel HH, Seifert E, Inglin R, Hagemann M, Vorburger SA, et al. Randomized controlled trial on single dose steroid before thyroidectomy for benign disease to improve postoperative nausea, pain, and vocal function. Ann Surg. 2008 Dec. 248(6):1060-6. [Medline].

  32. Zhang Y, Dong Z, Li J, Yang J, Yang W, Wang C. Comparison of endoscopic and conventional open thyroidectomy for Graves' disease: A meta-analysis. Int J Surg. 2017 Feb 22. 40:52-9. [Medline].

  33. [Guideline] Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017 Mar. 27 (3):315-89. [Medline]. [Full Text].

  34. FDA Drug Safety Communication: New Boxed Warning on severe liver injury with propylthiouracil. US Food and Drug Administration, April 21, 2010. Available at http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm209023.htm. Accessed: March 6, 2012.

  35. Yalamanchi S, Cooper DS. Thyroid disorders in pregnancy. Curr Opin Obstet Gynecol. 2015 Oct 19. [Medline].

  36. Burches-Feliciano MJ, Argente-Pla M, Garcia-Malpartida K, Rubio-Almanza M, Merino-Torres JF. Hyperthyroidism induced by topical iodine. Endocrinol Nutr. 2015 Aug 12. [Medline].

  37. Brandt F. The long-term consequences of previous hyperthyroidism. A register-based study of singletons and twins. Dan Med J. 2015 Jun. 62 (6):[Medline].

  38. Srinivasan S, Misra M. Hyperthyroidism in children. Pediatr Rev. 2015 Jun. 36 (6):239-48. [Medline].

Source: https://www.medscape.com/answers/121865-25170/what-is-the-role-of-thyrotropin-releasing-hormone-trh-in-the-pathogenesis-of-hyperthyroidism

Thyrotropin-releasing hormone | You and Your Hormones from the Society for Endocrinology

Thyrotropin-Releasing Hormone (TRH) Roles & Regulation

Thyrotropin-releasing hormone is one of the smallest hormones in the body, consisting of a miniature chain of just three amino acid building blocks. It is made by a cluster of nerve cells in the hypothalamus, an area at the base of the brain just above the pituitary gland.

This nerve cell cluster is known as the paraventricular nucleus. The nerve fibres that come it carry the thyrotropin-releasing hormone and release it into the blood surrounding the pituitary gland, where it has its most important action.

 This is to regulate the formation and secretion of thyroid stimulating hormone in the pituitary gland, which in turn regulates the production of thyroid hormones in the thyroid gland.

 Thyrotropin-releasing hormone is very short-lived, lasting for a matter of two minutes and travelling less than an inch in the bloodstream to the pituitary gland before it is broken down.

Secretion of thyrotropin-releasing hormone by the hypothalamus can also stimulate the release of another hormone from the pituitary gland, prolactin.

 Apart from its role in control of thyroid stimulating hormone and prolactin release, thyrotropin-releasing hormone has a wider distribution in tissues of the nervous system where it may act as a neurotransmitter.

For instance, an injection of thyrotropin-releasing hormone has effects on the arousal and feeding centres of the brain, causing wakefulness and loss of appetite. 

How is thyrotropin-releasing hormone controlled?

As its name implies, the main effect of thyrotropin-releasing hormone is to stimulate the release of thyrotropin (also known as thyroid stimulating hormone) from the pituitary gland.

Thyrotropin-releasing hormone is the master regulator of thyroid gland growth and function (including the secretion of the thyroid hormones thyroxine and triiodothyronine). These hormones control the body’s metabolic rate, heat generation, neuromuscular function and heart rate, among other things.

If there is insufficient thyroid hormone available for the brain, this will be detected by the hypothalamus and thyrotropin-releasing hormone will be released into the blood supplying the pituitary gland.

 The effect of thyrotropin-releasing hormone on the pituitary gland is to trigger thyroid stimulating hormone release, which, in turn stimulates the thyroid gland to make more thyroid hormone. In summary, thyrotropin-releasing hormone is the brain’s first messenger signal in the many actions controlling thyroid hormone secretions. 

Thyrotropin-releasing hormone (in its pharmaceutical formulation of 'protirelin') was widely used as a drug to test whether someone had thyroid overactivity.

 However, there are now more sensitive measurements that can detect very low levels of thyroid stimulating hormone in the blood.

 Thyrotropin-releasing hormone tests are still occasionally carried out but are normally used for the diagnosis of conditions caused by resistance to thyroid hormone action.

What happens if I have too much thyrotropin-releasing hormone?

There is no known case of too much thyrotropin-releasing hormone.

What happens if I have too little thyrotropin-releasing hormone?

If a person has too little thyrotropin-releasing hormone, they will develop thyroid underactivity (hypothyroidism). This is a rare condition, usually due to an injury or tumour which destroys this area of the hypothalamus. This situation is referred to as secondary or central hypothyroidism. 

Last reviewed: Mar 2018

Source: https://www.yourhormones.info/hormones/thyrotropin-releasing-hormone/

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