query: what type of hormone is thyrotropin releasing hormone

pos: Thyrotropin-releasing hormone of metabolic and hormonal functions. Side effects after intravenous TRH administration are minimal. Nausea, flushing, urinary urgency, and mild rise in blood pressure have been reported. After intrathecal administration, shaking, sweating, shivering, restlessness, and mild rise in blood pressure were observed. TRH belongs to a family of several thyrotropin-releasing hormones. Thyrotropin-releasing hormone Thyrotropin-releasing hormone (TRH), also called thyrotropin-releasing factor (TRF) or thyroliberin, is a releasing hormone, produced by the hypothalamus, that stimulates the release of thyrotropin (thyroid-stimulating hormone or TSH) and prolactin from the anterior pituitary. It is a tropic, tripeptidal hormone. TRH has been used clinically for the treatment

pos: Thyrotropin-releasing hormone Thyrotropin-releasing hormone Thyrotropin-releasing hormone (TRH), also called thyrotropin-releasing factor (TRF) or thyroliberin, is a releasing hormone, produced by the hypothalamus, that stimulates the release of thyrotropin (thyroid-stimulating hormone or TSH) and prolactin from the anterior pituitary. It is a tropic, tripeptidal hormone. TRH has been used clinically for the treatment of spinocerebellar degeneration and disturbance of consciousness in humans. Its pharmaceutical form is called protirelin (INN) (). TRH is produced by the globe in medial neurons of the paraventricular nucleus. At the beginning, it is synthesized as a 242-amino acid precursor polypeptide that contains 6 copies of the sequence -Gln-His-Pro-Gly-,

neg: Cyril Y. Bowers CY, Bouillon R. Growth Hormone Releasing Peptide 2 Infusion Synchronizes Growth Hormone, Thyrotropin and Prolactin Secretion in Prolonged Critical Illness. J Clin Endocrinol Metab 1997; 47:599-612. 6. Pihoker C, Kearns GL, French D, Bowers CY. Pharmacokinetics and Pharmacodynamics of Growth Hormone Releasing Peptide-2: A Phase I Study in Children J Clin Endocrinol Metab 1998; 83:1168-72. 7. Van den Berghe G, de Zegher F, Baxter RC, Veldhuis JD, Wouters P, Schetz M, Verwaest C, Van der Vorst E, Lauwers P, Bouillon R, Bowers CY. Neuroendocrinology of Prolonged Critical Illness: Effects of Exogenous Thyrotropin Releasing Hormone and Its Combination with Growth Hormone

neg: Prolactin-releasing hormone Prolactin-releasing hormone Prolactin-releasing hormone, also known as PRLH, is a hypothetical human hormone or hormone releasing factor. Existence of this factor has been hypothesized as prolactin is the only currently known hormone for which almost exclusively negative regulating factors are known (such as dopamine, leukemia inhibitory factor, some prostaglandins) but few stimulating factors. While many prolactin stimulating and enhancing factors are well known (such as thyrotropin-releasing hormone, oxytocin, vasoactive intestinal peptide and estrogen) those have primary functions other than stimulating prolactin release and the search for hypothetical releasing factor or factors continues. The prolactin-releasing peptide identified in 1998 was a

neg: Endocrine gland and inhibits glucose uptake and metabolism. Secretion is regulated by growth hormone releasing hormone (GHRH) and growth hormone inhibiting hormone (GHIH), or somatostatin. Hypersecretion causes gigantism in children and acromegaly in adults; hyposecretion in children causes pituitary dwarfism. Thyroid-stimulating hormone (TSH) promotes normal development and activity of the thyroid gland. Thyrotropin-releasing hormone (TRH) stimulates its release; negative feedback of thyroid hormone inhibits it. Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to release corticosteroids. ACTH release is triggered by corticotropin-releasing hormone (CRH) and inhibited by rising glucocorticoid levels. The gonadotropins—follicle-stimulating hormone (FSH) and luteinizing hormone (LH) regulate the functions of the

neg: Prolactin-releasing hormone candidate for this function, however as of 2008 it appears its function is not yet completely elucidated. Prolactin-releasing hormone Prolactin-releasing hormone, also known as PRLH, is a hypothetical human hormone or hormone releasing factor. Existence of this factor has been hypothesized as prolactin is the only currently known hormone for which almost exclusively negative regulating factors are known (such as dopamine, leukemia inhibitory factor, some prostaglandins) but few stimulating factors. While many prolactin stimulating and enhancing factors are well known (such as thyrotropin-releasing hormone, oxytocin, vasoactive intestinal peptide and estrogen) those have primary functions other than stimulating prolactin release and

neg: Hypopituitarism secretes a number of releasing hormones, often according to a circadian rhythm, into blood vessels that supply the anterior pituitary; most of these are stimulatory (thyrotropin-releasing hormone, corticotropin-releasing hormone, gonadotropin-releasing hormone and growth hormone-releasing hormone), apart from dopamine, which suppresses prolactin production. In response to the releasing hormone rate, the anterior pituitary produces its hormones (TSH, ACTH, LH, FSH, GH) which in turn stimulate effector hormone glands in the body, while prolactin (PRL) acts directly on the breast gland. Once the effector glands produce sufficient hormones (thyroxine, cortisol, estradiol or testosterone and IGF-1), both the hypothalamus and the pituitary cells

neg: Prolactin and a large number of cytokine receptors. Pituitary prolactin secretion is regulated by endocrine neurons in the hypothalamus. The most important of these are the neurosecretory tuberoinfundibulum (TIDA) neurons of the arcuate nucleus that secrete dopamine (aka Prolactin Inhibitory Hormone) to act on the D receptors of lactotrophs, causing inhibition of prolactin secretion. Thyrotropin-releasing factor (thyrotropin-releasing hormone) has a stimulatory effect on prolactin release, however prolactin is the only adenohypophyseal hormone whose principal control is inhibitory. Several variants and forms are known per species. Many fish have variants "prolactin A" and "prolactin B". Most vertebrates including humans also have the

neg: Hypothalamus evidence for central actions of prolactin. Findings have suggested that thyroid hormone (T4) is taken up by the hypothalamic glial cells in the infundibular nucleus/ median eminence, and that it is here converted into T3 by the type 2 deiodinase (D2). Subsequent to this, T3 is transported into the thyrotropin-releasing hormone (TRH)-producing neurons in the paraventricular nucleus. Thyroid hormone receptors have been found in these neurons, indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed MCT8, a thyroid hormone transporter, supporting the theory that T3 is transported into them. T3 could then bind to the

neg: Neuroendocrinology directly from the nerve endings of hypothalamic neurons. The first of these factors to be identified are thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (GnRH). TRH is a small peptide that stimulates the secretion of thyroid-stimulating hormone; GnRH (also called luteinizing hormone-releasing hormone) stimulates the secretion of luteinizing hormone and follicle-stimulating hormone. Roger Guillemin, a medical student of Faculté de Médecine of Lyon, and Andrew W. Schally of Tulane University isolated these factors from the hypothalamus of sheep and pigs, and then identified their structures. Guillemin and Schally were awarded the Nobel Prize in Physiology and Medicine in 1977 for their

neg: Paraventricular nucleus of hypothalamus their hormones at the primary capillary plexus of the hypophyseal portal system. The median eminence contains fiber terminals from many hypothalamic neuroendocrine neurons, secreting different neurotransmitters or neuropeptides, including vasopressin, corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH), gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GHRH), dopamine (DA) and somatostatin (growth hormone release inhibiting hormone, GIH) into blood vessels in the hypophyseal portal system. The blood vessels carry the peptides to the anterior pituitary gland, where they regulate the secretion of hormones into the systemic circulation. The parvocellular neurosecretory cells include those that make: As well as neuroendocrine neurons, the PVN contains interneurons

neg: Hypophyseal portal system Hypophyseal portal system The hypophyseal portal system is a system of blood vessels in the microcirculation at the base of the brain, connecting the hypothalamus with the anterior pituitary. Its main function is to quickly transport and exchange hormones between the hypothalamus arcuate nucleus and anterior pituitary gland. The capillaries in the portal system are fenestrated (have many small channels with high vascular permeability) which allows a rapid exchange between the hypothalamus and the pituitary. The main hormones transported by the system include gonadotropin-releasing hormone, corticotropin-releasing hormone, growth hormone–releasing hormone, and thyrotropin-releasing hormone. The blood supply and direction of flow

neg: Cyril Y. Bowers Baxter RC, Veldhuis JD, Bowers CY, Bouillon R. Reactivation of Pituitary Hormone Release and Metabolic Improvement by Infusion of Growth Hormone Releasing Peptide and Thyrotropin Releasing Hormone in Patients with Protracted Critical Illness. J Clin Endocrinol Metab 1999; 84:2140-50. 12. Meacham LR, Culler FL, Abdul-Latif H, Sullivan KM, Bowers CY. Preservation of Growth Hormone Releasing Peptide-2 During Prednisone Therapy Metabolism 1999; 48(5):585-89. 13. Bowers CY. GH Releasing Peptides (GHRPs). In: Handbook of Physiology, Kostyo J, Goodman H, eds, Oxford University Press, New York, 1999; pg 267-297. 14. Bowers CY. GHRP Historical Perspective Basic and Clinical. In: Human Growth Hormone Basic

neg: Median eminence as "hypophysiotropic hormones") collect before entering the portal system emptying into the general circulation. Such hypophysiotropic hormones include: CRF (corticotropin-releasing factor), GnRH (gonadotropin-releasing hormone), TRH (thyrotropin-releasing hormone), GHRH (growth hormone-releasing hormone), and DA (dopamine). These hypophysiotropic hormones stimulate or inhibit the release of hormones from the anterior pituitary. Further, anatomical evidence exists for bidirectional communication between the median eminence and the arcuate and ventromedial nucleus of the hypothalamus. Median eminence The median eminence, part of the inferior boundary of the hypothalamus in the brain, is attached to the infundibulum. The median eminence is a small swelling on the tuber cinereum,

neg: Corticotropin-releasing hormone binding protein family Corticotropin-releasing hormone binding protein family Corticotropin-releasing factor binding protein family consists of several eukaryotic corticotropin-releasing factor binding proteins (CRF-BP or CRH-BP). Corticotropin-releasing hormone (CRH) plays multiple roles in vertebrate species. In mammals, it is the major hypothalamic releasing factor for pituitary adrenocorticotropin secretion, and is a neurotransmitter or neuromodulator at other sites in the central nervous system. In non-mammalian vertebrates, CRH not only acts as a neurotransmitter and hypophysiotropin, it also acts as a potent thyrotropin-releasing factor, allowing CRH to regulate both the adrenal and thyroid axes, especially in development. Corticotropin-releasing factor binding protein (CRH-BP) is thought to play an

neg: Hypothalamic–pituitary–thyroid axis Hypothalamic–pituitary–thyroid axis The hypothalamic–pituitary–thyroid axis (HPT axis for short, a.k.a. thyroid homeostasis or thyrotropic feedback control) is part of the neuroendocrine system responsible for the regulation of metabolism. As its name suggests, it depends upon the hypothalamus, the pituitary gland, and the thyroid gland. The hypothalamus senses low circulating levels of thyroid hormone (Triiodothyronine (T3) and Thyroxine (T4)) and responds by releasing thyrotropin-releasing hormone (TRH). The TRH stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH). The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback

neg: Hypothalamus thyroid hormone receptor in these neurons and affect the production of thyrotropin-releasing hormone, thereby regulating thyroid hormone production. The hypothalamus functions as a type of thermostat for the body. It sets a desired body temperature, and stimulates either heat production and retention to raise the blood temperature to a higher setting or sweating and vasodilation to cool the blood to a lower temperature. All fevers result from a raised setting in the hypothalamus; elevated body temperatures due to any other cause are classified as hyperthermia. Rarely, direct damage to the hypothalamus, such as from a stroke, will cause a fever;

neg: Prolyl endopeptidase Prolyl endopeptidase Prolyl endopeptidase (PE) also known as prolyl oligopeptidase or post-proline cleaving enzyme is an enzyme that in humans is encoded by the "PREP" gene. Prolyl endopeptidase is a large cytosolic enzyme that belongs to a distinct class of serine peptidases. It was first described in the cytosol of rabbit brain as an oligopeptidase, which degrades the nonapeptide bradykinin at the Pro-Phe bond. The enzyme is involved in the maturation and degradation of peptide hormones and neuropeptides such as alpha-melanocyte-stimulating hormone, luteinizing hormone-releasing hormone (LH-RH), thyrotropin-releasing hormone, angiotensin, neurotensin, oxytocin, substance P and vasopressin. PREP cleaves peptide bonds at

neg: Hypothalamic–pituitary–thyroid axis these animals. The pituitary gland secretes thyrotropin (TSH; Thyroid Stimulating Hormone) that stimulates the thyroid to secrete thyroxine (T4) and, to a lesser degree, triiodothyronine (T3). The major portion of T3, however, is produced in peripheral organs, e.g. liver, adipose tissue, glia and skeletal muscle by deiodination from circulating T4. Deiodination is controlled by numerous hormones and nerval signals including TSH, vasopressin and catecholamines. Both peripheral thyroid hormones (iodothyronines) inhibit thyrotropin secretion from the pituitary (negative feedback). Consequently, equilibrium concentrations for all hormones are attained. TSH secretion is also controlled by thyrotropin releasing hormone (thyroliberin, TRH), whose secretion itself is

neg: Somatostatin receptor 2 the bowels.This inhibition by somatostatin allows the body to uptake the maximum amount of nutrients in the digestive system. Along with the gut and pancreas, SSTR2 also inhibits secretion of neurotransmitters in the central and peripheral nervous system. These hormones include dopamine, norpinephrine, thyrotropin-releasing hormone, and corticotropin-releasing hormone. Many of these hormones help the body maintain homeostasis or react properly to a stimulus such as something pleasurable or a stress in the environment. Because of which, the receptors for somatostatin type 2 impact the body's locomotor, sensory, autonomic, and cognitive functions. Somatostatin receptor 2 has been shown to interact with

neg: Hypothalamic disease normal functioning of the pituitary. Hypothalamic disease may cause insufficient or inhibited signalling to the pituitary leading to deficiencies of one or more of the following hormones: thyroid-stimulating hormone, adrenocorticotropic hormone, beta-endorphin, luteinizing hormone, follicle-stimulating hormone, and melanocyte–stimulating hormones. Treatment for hypopituitarism involves hormone replacement therapy. Neurogenic diabetes insipidus may occur due to low levels of ADH production from the hypothalamus. Insufficient levels of ADH result in increased thirst and urine output, and prolonged excessive urine excretion increases the risk of dehydration. The thyroid gland is an auxiliary organ to the hypothalamus-pituitary system. Thyrotropin-releasing hormone (TRH) produced by the hypothalamus

neg: Thyroid hormone resistance this chain can result in thyroid hormone resistance. The most common cause of the syndrome are mutations of the β (beta) form ("THRB" gene) of the thyroid hormone receptor, of which over 100 different mutations have been documented. Mutations in "MCT8" and "SECISBP2" have also been associated with this condition. Hypothalamus secretes a hormone called thyrotropin releasing hormone (TRH) which in turn release thyroid stimulating hormone (TSH). TSH signals thyroid to secrete thyroid hormones thyroxine (T4) and triiodothyronine (T3). T4 gets converted to active T3 in peripheral tissues with the help of deiodinase enzymes. T3 negatively feedback on the pituitary

neg: Hypothyroidism a key role in maintaining thyroid hormone levels within normal limits. Production of TSH by the anterior pituitary gland is stimulated in turn by thyrotropin-releasing hormone (TRH), released from the hypothalamus. Production of TSH and TRH is decreased by thyroxine by a negative feedback process. Not enough TRH, which is uncommon, can lead to not enough TSH and thereby to not enough thyroid hormone production. Pregnancy leads to marked changes in thyroid hormone physiology. The gland is increased in size by 10%, thyroxine production is increased by 50%, and iodine requirements are increased. Many women have normal thyroid function but

neg: Pituitary-specific positive transcription factor 1 for high affinity DNA binding on genes encoding growth hormone (GH; MIM 139250) and prolactin (PRL; MIM 176760). PIT1 is also important for regulation of the genes encoding prolactin and thyroid-stimulating hormone beta subunit (TSHB; MIM 188540) by thyrotropin-releasing hormone (TRH; MIM 257120) and cyclic AMP.[supplied by OMIM] Pituitary-specific positive transcription factor 1 has been shown to interact with GATA2 and PITX1. Pituitary-specific positive transcription factor 1 POU domain, class 1, transcription factor 1 (Pit1, growth hormone factor 1), also known as POU1F1, is a transcription factor for growth hormone. PIT1 is a pituitary-specific transcription factor responsible for pituitary development

neg: G protein-coupled receptor glutamate (metabotropic effect); glucagon; acetylcholine (muscarinic effect); chemokines; lipid mediators of inflammation (e.g., prostaglandins, prostanoids, platelet-activating factor, and leukotrienes); peptide hormones (e.g., calcitonin, C5a anaphylatoxin, follicle-stimulating hormone [FSH], gonadotropin-releasing hormone [GnRH], neurokinin, thyrotropin-releasing hormone [TRH], and oxytocin); and endocannabinoids. GPCRs that act as receptors for stimuli that have not yet been identified are known as orphan receptors. However, in other types of receptors that have been studied, wherein ligands bind externally to the membrane, the ligands of GPCRs typically bind within the transmembrane domain. However, protease-activated receptors are activated by cleavage of part of their extracellular domain. The transduction of

neg: Derek George Smyth 4-Phenyl-3-butenoic acid, an in vivo inhibitor of peptidylglycine hydroxylase (peptide amidating enzyme). Eur.J.Biochem., 189, 363-368. 50. Cockle, S,M., Aitken, A., Beg, F. and Smyth, D.G. (1989) A novel peptide, pyroglutamylglutamylproline amide,in the rabbit prostate complex, structurally related to thyrotropin releasing hormone. J. Biol. Chem., 264, 7788-7791 51. Khan, Z., Aitken,A., del Rio-Garcia, J. and Smyth, D.G. (1992) Isolation and identification of two neutral thyrotropin hormone-like peptides, pyroglutamylphenylalanine proline amide and pyroglutamylglutamine proline amide from human seminal fluid. J. Biol. Chem., 267, 7464-7469. 52. Cockle, S.M., Aitken, A., Beg, F. and Smyth, D.G. (1989) The TRH-related peptide pyroglutamylglutamylproline amide is present

neg: Thyroid-stimulating hormone thyroxine (T), which has only a slight effect on metabolism. T is converted to triiodothyronine (T), which is the active hormone that stimulates metabolism. About 80% of this conversion is in the liver and other organs, and 20% in the thyroid itself. TSH is secreted throughout life but particularly reaches high levels during the periods of rapid growth and development, as well as in response to stress. The hypothalamus, in the base of the brain, produces thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary gland to produce TSH. Somatostatin is also produced by the hypothalamus, and has an opposite effect

neg: Thyroid hormones T3 and T4, as well as the non-coupled tyrosine derivatives MIT and DIT. The hormones T and T are the biologically active agents central to metabolic regulation. Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T. T is converted as required in the tissues by iodothyronine deiodinase. Deficiency of deiodinase can mimic hypothyroidism due to iodine deficiency. T is more active than T, though it is present in less quantity than T. Thyrotropin-releasing hormone (TRH) is released from hypothalamus by 6 – 8 weeks, and thyroid-stimulating hormone (TSH) secretion from

neg: Thyrotropin-releasing hormone a peptide. Guillemin's chemist began concurring with these results in 1969, as NIH threatened to cut off funding for the project, leading both parties to return to work on synthesis. Schally and Guillemin shared the 1977 Nobel Prize in Medicine ""for their discoveries concerning the peptide hormone production of the brain."" News accounts of their work often focused on their "fierce competition" and use of a very large amount of sheep and pig brains to locate the hormone. Its molecular weight is 359.5 Da. Its tripeptide structure is: (pyro)Glu-His-Pro-NH. Its logp octanol/water is -2.46 TRH is used clinically by intravenous

neg: Neuroendocrinology its product?" and "how is information encoded in electrical activity?"[It appears that this is a primary source observation.] The pituitary gland is divided into two sections: the anterior pituitary and the posterior pituitary. The hypothalamus controls the anterior pituitary's hormone secretion by sending trophic hormones down the hypothalamohypophysial portal system. For example, thyrotropin-releasing hormone stimulates the secretion of thyroid-stimulating hormone by the anterior pituitary. The posterior pituitary is innervated by the hypothalamus; the hormones oxytocin and vasopressin are synthesized by neuroendocrine cells in the hypothalamus and stored at the nerves' ends in the posterior pituitary. They are secreted directly into

neg: Wylie Vale Wylie Vale Wylie Walker Vale Jr. (July 3, 1941 – January 3, 2012) was an American endocrinologist who helped identify hormones controlling basic bodily functions. Vale was born in Houston, Texas, on July 3, 1941. He completed a B.A. degree in biology at Rice University and obtained a Ph.D. in physiology and biochemistry from Baylor College of Medicine. He commenced employment at the Salk Institute for Biological Studies in San Diego, California, in 1970. In collaboration with his advisor and mentor Roger Guillemin, Vale contributed to the discovery, isolation and identification of thyrotropin releasing hormone and gonadotropin-releasing hormone in the

neg: Thyrotropin-releasing hormone Following secretion, TRH travels across the median eminence to the anterior pituitary gland via the hypophyseal portal system where it stimulates the release of thyroid-stimulating hormone from cells called thyrotropes. TRH can also be detected in other areas of the body including the gastrointestinal system and pancreatic islets, as well as in the brain. The seleke of TRH was first determined, and the hormone synthesized, by Roger Guillemin and Andrew V. Schally in 1969. Both parties insisted their labs determined the sequence first: Schally first suggested the possibility in 1966, but abandoned it after Guillemin proposed TRH was not actually

neg: Breast development extension adrenocorticotropic hormone (ACTH)), and thyroid hormones such as thyroxine (and by extension thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH)) also play permissive but less well-understood/poorly-characterized roles in breast development during both puberty and pregnancy, and are required for full functional development. Leptin has also been found to be an important factor in mammary gland development, and has been found to promote mammary epithelial cell proliferation. In contrast to the female-associated sex hormones, estrogen and progesterone, the male-associated sex hormones, the androgens, such as testosterone and dihydrotestosterone (DHT), powerfully suppress the action of estrogen in the breasts. At least one

neg: IGSF1 The "IGSF1" gene is also active in the brain and in the developing liver. It can also become reactivated in liver cancer (hepatocellular carcinoma). Mice lacking a functional "Igsf1" gene similarly exhibit hypothyroidism of central origin. The "IGSF1" gene is particularly active in the pituitary gland. The pituitary synthesizes and secretes thyroid-stimulating hormone (TSH). TSH, in turn, stimulates production of the thyroid hormones, thyroxine and triiodothyronine, by the thyroid gland. TSH secretion is controlled by thyrotropin-releasing hormone (TRH), which is released by neurons in the hypothalamus of the brain. In "Igsf1" deficient mice, the receptor for TRH is downregulated in

neg: Thyrotropin receptor intracellular levels of cAMP rise. cAMP activates all functional aspects of the thyroid cell, including iodine pumping; thyroglobulin synthesis, iodination, endocytosis, and proteolysis; thyroid peroxidase activity; and hormone release. Thyrotropin receptor The thyrotropin receptor (or TSH receptor) is a receptor (and associated protein) that responds to thyroid-stimulating hormone (also known as "thyrotropin") and stimulates the production of thyroxine (T4) and triiodothyronine (T3). The TSH receptor is a member of the G protein-coupled receptor superfamily of integral membrane proteins and is coupled to the G protein. It is primarily found on the surface of the thyroid epithelial cells, but also found

neg: Thyroid (TSH) secreted from the anterior pituitary gland, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus. The thyroid may be affected by several diseases. Hyperthyroidism occurs when the gland produces excessive amounts of thyroid hormones, the most common cause being Graves' disease, an autoimmune disorder. In contrast, hypothyroidism is a state of insufficient thyroid hormone production. Worldwide, the most common cause is iodine deficiency. Thyroid hormones are important for development, and hypothyroidism secondary to iodine deficiency remains the leading cause of preventable intellectual disability. In iodine-sufficient regions, the most common cause of hypothyroidism is Hashimoto's thyroiditis, also

neg: Galactorrhea and thyroid conditions with elevated levels of thyroid-stimulating hormone (TSH) or thyrotropin-releasing hormone (TRH). No obvious cause is found in about 50% of cases. Lactation requires the presence of prolactin, and the evaluation of galactorrhea includes eliciting a history for various medications or foods (methyldopa, opioids, antipsychotics, serotonin reuptake inhibitors, as well as licorice) and for behavioral causes (stress, and breast and chest wall stimulation), as well as evaluation for pregnancy, pituitary adenomas (with overproduction of prolactin or compression of the pituitary stalk), and hypothyroidism. Adenomas of the anterior pituitary are most often prolactinomas. Overproduction of prolactin leads to cessation

neg: Corticotropin-releasing hormone receptor Corticotropin-releasing hormone receptor Corticotropin-releasing hormone receptors (CRHRs), also known as corticotropin-releasing factor receptors (CRFRs) are a G protein-coupled receptor family that binds corticotropin-releasing hormone (CRH). There are two receptors in the family, designated as type 1 and 2, each encoded by a separate gene ( and respectively). CRHRs are important mediators in the stress response. Cells in the anterior lobe of the pituitary gland known as corticotropes express the receptors and will secrete adrenocorticotropic hormone (ACTH) when stimulated. This binding of corticotropin releasing-hormone (CRH) activates the hypothalamic-pituitary-adrenal (HPA) axis, one of the two parts of the fight-or-flight response to stress.

neg: Euthyroid sick syndrome The balance of D2 and D3 is important for overall T3/rT3 balance. In NTIS, the concentrations of these deiodinases are altered, although it is unclear whether NTIS is the cause or effect of this in peripheral tissues; in some studies, the alterations in thyroid hormone concentrations occurred before the changes in deiodinase activity. Typically, peripheral D1 and D2 are downregulated, while peripheral D3 is upregulated; this is associated with lower T4 and increased rT3. Thyrotropin Releasing Hormone (TRH) neurons in the hypothalamus integrate global signals about the body’s energy state. They may be stimulated by signals such as leptin, alpha-MSH,

neg: Thyroid from the gland are about 80–90% T and about 10–20% T. Deiodinase enzymes in peripheral tissues remove the iodine from MIT and DIT and convert T to T and RT This is a major source of both RT (95%) and T (87%) in peripheral tissues. The production of thyroxine and triiodothyronine is primarily regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary gland. TSH release in turn is stimulated by thyrotropin releasing hormone (TRH), released in a pulsatile manner from the hypothalamus. The thyroid hormones provide negative feedback to the thyrotropes TSH and TRH: when the thyroid hormones are

neg: Homologous desensitization be degraded by lysosomes or reinserted into the plasma membrane, which is called receptor recycling. Post-translational modification also affects receptor endocytosis. For example, different glycosylations on the exterior N-terminus of dopamine receptors D and D were associated with specific endocytotic pathways. Additionally, palmitoylation, which primarily mediates receptor localization within the membrane, can also affect endocytosis. It is required for the endocytosis of thyrotropin-releasing hormone and D receptors, and it is inhibitory for leutinizing hormone and vasopressin receptor 1A receptors. It has been shown to have no effect on adrenergic receptors (specifically ß and α). Homologous desensitization Homologous desensitization occurs when

neg: Corticotropin-releasing hormone receptor 2 more potent at stimulating CRHR2 beta than CRHR2 alpha and CRHR2 gamma, suggesting that the N-terminal sequence is involved in the ligand-receptor interaction. Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling

neg: Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling via guanine nucleotide-binding proteins (G proteins) and downstream effectors such as adenylate cyclase. The CRF receptor is a multi-pass membrane protein with a

neg: Thyroid function tests Thyroid function tests Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. TFTs may be requested if a patient is thought to suffer from hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid), or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requested routinely in conditions linked to thyroid disease, such as atrial fibrillation and anxiety disorder. A TFT panel typically includes thyroid hormones such as thyroid-stimulating hormone (TSH, thyrotropin) and thyroxine (T4), and triiodothyronine (T3) depending on local laboratory policy. Thyroid-stimulating hormone (TSH, thyrotropin) is

neg: Gonadotropin-releasing hormone agonist Gonadotropin-releasing hormone agonist A gonadotropin-releasing hormone agonist (GnRH agonist) is a type of medication which affects gonadotropins and sex hormones. They are used for a variety of indications including in fertility medicine and to lower sex hormone levels in the treatment of hormone-sensitive cancers such as prostate cancer and breast cancer, certain gynecological disorders like heavy periods and endometriosis, high testosterone levels in women, early puberty in children, as a part of transgender hormone therapy, and to delay puberty in transgender youth among other uses. GnRH agonists are given by injections into fat, as implants placed into fat, and as

neg: Gonadotropin-releasing hormone modulator Gonadotropin-releasing hormone modulator A GnRH modulator, or GnRH receptor modulator, is a type of medication which modulates the GnRH receptor, the biological target of the hypothalamic hormone gonadotropin-releasing hormone (GnRH). They include GnRH agonists and GnRH antagonists. These medications may be GnRH analogues like leuprorelin and cetrorelix – peptides that are structurally related to GnRH – or small-molecules like elagolix, which are structurally distinct from GnRH analogues. GnRH modulators affect the secretion of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn affects the gonads, influencing their function and hence fertility as well as the production of

neg: Thyroid thyroglossal duct. At the end of the fifth week the thyroglossal duct degenerates and the detached thyroid continues on to its final position over the following two weeks. The fetal hypothalamus and pituitary start to secrete thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH). TSH is first measurable at 11 weeks. By 18–20 weeks, the production of thyroxine (T) reaches a clinically significant and self-sufficient level. Fetal triiodothyronine (T) remains low, less than 15 ng/dL until 30 weeks, and increases to 50 ng/dL at full-term. The fetus needs to be self-sufficient in thyroid hormones in order to guard against neurodevelopmental disorders

neg: Endocrinology combination of two iodinated tyrosine amino acid residues. Peptide hormones and protein hormones consist of three (in the case of thyrotropin-releasing hormone) to more than 200 (in the case of follicle-stimulating hormone) amino acid residues and can have a molecular mass as large as 30,000 grams per mole. All hormones secreted by the pituitary gland are peptide hormones, as are leptin from adipocytes, ghrelin from the stomach, and insulin from the pancreas. Steroid hormones are converted from their parent compound, cholesterol. Mammalian steroid hormones can be grouped into five groups by the receptors to which they bind: glucocorticoids, mineralocorticoids, androgens,

neg: Thyroid-stimulating hormone Thyroid-stimulating hormone Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, TSH, or hTSH for human TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T), and then triiodothyronine (T) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid. In 1916, Bennett M. Allen and Philip E. Smith found that the pituitary contained a thyrotropic substance. TSH (with a half life of about an hour) stimulates the thyroid gland to secrete the hormone

neg: Thyroid-stimulating hormone manufactured by Genzyme Corp under the trade name Thyrogen. It is used to manipulate endocrine function of thyroid-derived cells, as part of the diagnosis and treatment of thyroid cancer. Thyroid-stimulating hormone Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, TSH, or hTSH for human TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T), and then triiodothyronine (T) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid. In 1916, Bennett M. Allen

neg: Releasing and inhibiting hormones Releasing and inhibiting hormones Releasing hormones and inhibiting hormones are hormones whose main purpose is to control the release of other hormones, either by stimulating or inhibiting their release. They are also called liberins () and statins () (respectively), or releasing factors and inhibiting factors. The examples are hypothalamic-pituitary hormones that can be classified from several viewpoints: they are hypothalamic hormones (originating in the hypothalamus), they are hypophysiotropic hormones (affecting the hypophysis, that is, the pituitary gland), and they are tropic hormones (having other endocrine glands as their target). For example, thyrotropin-releasing hormone (TRH) is released from the hypothalamus in

neg: Corticotropin-releasing hormone antagonist Corticotropin-releasing hormone antagonist A Corticotropin-Releasing Hormone Antagonist (CRH antagonist) is a specific type of receptor antagonist that blocks the receptor sites for Corticotropin-releasing hormone (also known as Corticotropin-releasing factor (CRF)), which synchronizes the behavioral, endocrine, autonomic, and immune responses to stress by controlling the hypothalamic-pituitary-adrenal axis (HPA Axis). CRH Antagonists thereby block the consequent secretions of ACTH and cortisol due to stress, among other effects. There are four subtypes of the CRH receptor known at present, defined as CRF-1, CRF-2a, CRF-2b, and CRF-2g. Three of these receptors are expressed only in the brain: CRF-1 in the cortex and cerebrum, CRF-2a

neg: Derek George Smyth in human seminal fluid. FEBS Letts., 252, 113-117. 53. del Rio-Garcia, J. and Smyth, D.G. (1990) Distribution of pyroglutamylpeptide amides in the central nervous system and periphery of the rat. J. Endocrinol., 127, 445-450. 54. Bilek, R., Gkonos, P.J., Tavianini, M., Smyth, D.G. and Roos, B.A. (1992) The thyrotropin releasing hormone (TRH)-like peptides in rat prostate are not formed by expression of the TRH gene but are suppressed by thyroid hormone. J. Endocrinol., 132, 177-184. 55. Linden, H., del Rio-Garcia, J., Huber, A., Kreil, G. and Smyth, D.G. (1996) The TRH-like peptides in rabbit testis are different from the TRH-like

neg: Cyproterone acetate the breasts (80–90%) being represented by stromal or adipose tissue, and it is uncertain to what extent, if any, that development of lobuloalveolar structures (a type of epithelial tissue) contributes to breast size or shape. CPA has potent antigonadotropic effects via activation of the PR. It blunts the gonadotropin releasing hormone (GnRH)-induced secretion of gonadotropins, and accordingly, markedly suppresses circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) at sufficiently high dosages. Consequently, levels of progesterone, androstenedione, testosterone, DHT, and estradiol are also markedly lowered at sufficiently high dosages, while an elevation in sex hormone-binding globulin (SHBG) and prolactin

neg: Gonadotropin-releasing hormone modulator sex steroids, including that of estradiol and progesterone in women and of testosterone in men. As such, GnRH modulators can also be described as progonadotropic or antigonadotropic, depending on whether they act to increase or decrease gonadotropins. = Under development; not yet marketed. Gonadotropin-releasing hormone modulator A GnRH modulator, or GnRH receptor modulator, is a type of medication which modulates the GnRH receptor, the biological target of the hypothalamic hormone gonadotropin-releasing hormone (GnRH). They include GnRH agonists and GnRH antagonists. These medications may be GnRH analogues like leuprorelin and cetrorelix – peptides that are structurally related to GnRH – or

neg: Corticotropin-releasing hormone receptor CRHRs are also present in other brain areas such as the amygdala, locus coeruleus and hippocampus. Within the hippocampus, the CRHR1s are most abundant, residing mainly on the pyramidal cells of CA1 and CA3. Chronic activation of CRHR1s by CRH induced by early life stress has been shown to underlie memory deficits and learning impairments and anxiety in adulthood. Corticotropin-releasing hormone receptor Corticotropin-releasing hormone receptors (CRHRs), also known as corticotropin-releasing factor receptors (CRFRs) are a G protein-coupled receptor family that binds corticotropin-releasing hormone (CRH). There are two receptors in the family, designated as type 1 and 2, each encoded by

neg: Growth-hormone-releasing hormone receptor to date. Growth-hormone-releasing hormone receptor The growth-hormone-releasing hormone receptor (GHRHR) is a G-protein-coupled receptor that binds growth hormone-releasing hormone. The GHRHR activates a Gs protein that causes a cascade of cAMP via Adenylate cyclase. This gene, expressed in the pituitary, encodes a receptor for growth-hormone-releasing hormone. Binding of this hormone to the receptor leads to synthesis and release of growth hormone. Mutations in this gene have been associated with isolated growth-hormone deficiency (IGHD), also known as Dwarfism of Sindh, a disorder characterized by short stature. Many alternate transcriptional splice variants encoding different isoforms have been described, but only two have

neg: Growth-hormone-releasing hormone receptor Growth-hormone-releasing hormone receptor The growth-hormone-releasing hormone receptor (GHRHR) is a G-protein-coupled receptor that binds growth hormone-releasing hormone. The GHRHR activates a Gs protein that causes a cascade of cAMP via Adenylate cyclase. This gene, expressed in the pituitary, encodes a receptor for growth-hormone-releasing hormone. Binding of this hormone to the receptor leads to synthesis and release of growth hormone. Mutations in this gene have been associated with isolated growth-hormone deficiency (IGHD), also known as Dwarfism of Sindh, a disorder characterized by short stature. Many alternate transcriptional splice variants encoding different isoforms have been described, but only two have been characterized

neg: Corticotropin-releasing hormone has been shown to interact with corticotropin-releasing hormone receptor 1. Corticotropin-releasing hormone Corticotropin-releasing hormone (CRH) (also known as corticotropin-releasing factor (CRF) or corticoliberin; corticotropin may also be spelled corticotrophin) is a peptide hormone involved in the stress response. It is a releasing hormone that belongs to corticotropin-releasing factor family. In humans, it is encoded by the "CRH" gene. Its main function is the stimulation of the pituitary synthesis of ACTH, as part of the HPA Axis. Corticotropin-releasing hormone (CRH) is a 41-amino acid peptide derived from a 196-amino acid preprohormone. CRH is secreted by the paraventricular nucleus (PVN) of the

neg: Growth hormone–releasing hormone Growth hormone–releasing hormone Growth hormone–releasing hormone (GHRH), also known as somatocrinin or by several other names in its endogenous forms and as somatorelin (INN) in its pharmaceutical form, is a releasing hormone of growth hormone (GH). It is a 44-amino acid peptide hormone produced in the arcuate nucleus of the hypothalamus. GHRH first appears in the human hypothalamus between 18 and 29 weeks of gestation, which corresponds to the start of production of growth hormone and other somatotropes in fetuses. GHRH is released from neurosecretory nerve terminals of these arcuate neurons, and is carried by the hypothalamo-hypophyseal portal system to

neg: Behavioral endocrinology to regulate their target cell's metabolism. These hormones are a product of the hypothalamic–pituitary–adrenal axis (HPA axis or HTPA axis). These organs function together as the hypothalamus releases thyrotropin releasing hormone (TRH), which cause the pituitary gland to secrete thyrotropin that signal the thyroid gland to process and release thyroxine and triiodothyronine to the body. These hormones play a major role in the Neuroendocrine system which regulates the vital body functions of breathing, body weight, heart rate, muscle strength, cholesterol levels, especially body temperature. When your body has to much or too little of these hormones it has abnormal affect

neg: Gonadotropin-releasing hormone Gonadotropin-releasing hormone Gonadotropin-releasing hormone (GnRH) is a releasing hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary. GnRH is a tropic peptide hormone synthesized and released from GnRH neurons within the hypothalamus. The peptide belongs to gonadotropin-releasing hormone family. It constitutes the initial step in the hypothalamic–pituitary–gonadal axis. The identity of GnRH was clarified by the 1977 Nobel Laureates Roger Guillemin and Andrew V. Schally: As is standard for peptide representation, the sequence is given from amino terminus to carboxyl terminus; also standard is omission of the designation of chirality, with assumption

neg: Corticotropin-releasing hormone Corticotropin-releasing hormone Corticotropin-releasing hormone (CRH) (also known as corticotropin-releasing factor (CRF) or corticoliberin; corticotropin may also be spelled corticotrophin) is a peptide hormone involved in the stress response. It is a releasing hormone that belongs to corticotropin-releasing factor family. In humans, it is encoded by the "CRH" gene. Its main function is the stimulation of the pituitary synthesis of ACTH, as part of the HPA Axis. Corticotropin-releasing hormone (CRH) is a 41-amino acid peptide derived from a 196-amino acid preprohormone. CRH is secreted by the paraventricular nucleus (PVN) of the hypothalamus in response to stress. Increased CRH production has been

neg: GHRP-6 GHRP-6 Growth hormone-releasing peptide 6 (GHRP-6) (developmental code name SKF-110679), also known as growth hormone-releasing hexapeptide, is one of several synthetic met-enkephalin analogues that include unnatural -amino acids, were developed for their growth hormone-releasing activity and are called growth hormone secretagogues. They lack opioid activity but are potent stimulators of growth hormone (GH) release. These secretagogues are distinct from growth hormone releasing hormone (GHRH) in that they share no sequence relation and derive their function through activation of a completely different receptor. This receptor was originally called the growth hormone secretagogue receptor (GHSR), but due to subsequent discoveries, the hormone

neg: Corticotropin-releasing hormone antagonist atopic dermatitis, which are often further exacerbated by HPA actication due to stress. There is also hope that CRH receptor antagonists could be useful in the treatment of a range of clinical disorders associated with abnormal stress responses, such as psychosocial growth retardation, euthyroid sick syndrome, stress-induced asthma, and psychogenic impotence. Further research on CRH-1 and CRH-2 receptor antagonists, as well as the mechanisms behind them, needs to be completed before further clinical aspirations can be properly considered. Corticotropin-releasing hormone antagonist A Corticotropin-Releasing Hormone Antagonist (CRH antagonist) is a specific type of receptor antagonist that blocks the receptor sites for

neg: Gonadotropin-releasing hormone grouped together, and will take significantly longer to retrieve their pups. The natural hormone is also used in veterinary medicine as a treatment for cattle with cystic ovarian disease. The synthetic analogue deslorelin is used in veterinary reproductive control through a sustained-release implant. As with many hormones, GnRH has been called by various names in the medical literature over the decades since its existence was first inferred. They are as follows: Gonadotropin-releasing hormone Gonadotropin-releasing hormone (GnRH) is a releasing hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary. GnRH is a tropic

neg: Gonadotropin-releasing hormone receptor Gonadotropin-releasing hormone receptor The gonadotropin-releasing hormone receptor (GnRHR), also known as the luteinizing hormone releasing hormone receptor (LHRHR), is a member of the seven-transmembrane, G-protein coupled receptor (GPCR) family. It is the receptor of gonadotropin-releasing hormone (GnRH). The GnRHR is expressed on the surface of pituitary gonadotrope cells as well as lymphocytes, breast, ovary, and prostate. This receptor is a 60 kDa G protein-coupled receptor and resides primarily in the pituitary and is responsible for eliciting the actions of GnRH after its release from the hypothalamus. Upon activation, the LHRHr stimulates tyrosine phosphatase and elicits the release of LH from

neg: Gonadotropin-releasing hormone receptor its effects on reproductive maturation. Understanding how GnRHR functions has been key to developing clinical strategies to treat reproductive-related disorders. Gonadotropin-releasing hormone receptor The gonadotropin-releasing hormone receptor (GnRHR), also known as the luteinizing hormone releasing hormone receptor (LHRHR), is a member of the seven-transmembrane, G-protein coupled receptor (GPCR) family. It is the receptor of gonadotropin-releasing hormone (GnRH). The GnRHR is expressed on the surface of pituitary gonadotrope cells as well as lymphocytes, breast, ovary, and prostate. This receptor is a 60 kDa G protein-coupled receptor and resides primarily in the pituitary and is responsible for eliciting the actions of GnRH

neg: Gonadotropin-releasing hormone agonist modeled after the natural GnRH decapeptide with specific modifications, usually double and single substitutions and typically in position 6 (amino acid substitution), 9 (alkylation) and 10 (deletion). These substitutions inhibit rapid degradation. Agonists with two substitutions include: leuprorelin, buserelin, histrelin, goserelin, and deslorelin. The agents nafarelin and triptorelin are agonists with single substitutions at position 6. GnRH analogues are also used in veterinary medicine. Uses include: Gonadotropin-releasing hormone agonist A gonadotropin-releasing hormone agonist (GnRH agonist) is a type of medication which affects gonadotropins and sex hormones. They are used for a variety of indications including in fertility medicine and to

neg: Gonadotropin-releasing hormone analogue reversible upon stopping the medication, it can be maintained when GnRH agonists use is continued for a long time. A gonadotropin-releasing hormone antagonist (GnRH antagonist) is an analogue that blocks the GnRH receptor resulting in an immediate drop in gonadotropin (FSH, LH) secretion. The GnRH antagonist is primarily used in IVF treatments to block natural ovulation. All GnRH analogues are contraindicated in pregnancy (pregnancy category X). Gonadotropin-releasing hormone analogue A gonadotropin-releasing hormone analogue (GnRH analogue or "analog"), also known as a luteinizing hormone releasing hormone agonist (LHRH agonist) or LHRH analogue is a synthetic peptide drug modeled after the human

neg: Gonadotropin-releasing hormone analogue Gonadotropin-releasing hormone analogue A gonadotropin-releasing hormone analogue (GnRH analogue or "analog"), also known as a luteinizing hormone releasing hormone agonist (LHRH agonist) or LHRH analogue is a synthetic peptide drug modeled after the human hypothalamic gonadotropin-releasing hormone (GnRH). A GnRH analogue is designed to interact with the GnRH receptor and modify the release of pituitary gonadotropins FSH and LH for therapeutic purposes. Shortly after the discovery of GnRH by Nobel laureates Guillemin and Schally researchers tried to modify the GnRH decapeptide with the intent to synthesize stimulating and blocking variants. Examples include goserelin and leuprorelin. An example of a GnRH

neg: Hypothyroidism (99.97%) is bound to plasma proteins such as thyroxine-binding globulin; only the free unbound thyroid hormone is biologically active. Overexpression of deiodinase can thus lead to consumptive hypothyroidism. The thyroid gland is the only source of thyroid hormone in the body; the process requires iodine and the amino acid tyrosine. Iodine in the bloodstream is taken up by the gland and incorporated into thyroglobulin molecules. The process is controlled by the thyroid-stimulating hormone (TSH, thyrotropin), which is secreted by the pituitary. Not enough iodine, or not enough TSH, can result in decreased production of thyroid hormones. The hypothalamic–pituitary–thyroid axis plays

neg: Corticotropin-releasing hormone receptor 1 II and urocortin III. Variations in the "CRHR1" gene is associated with enhanced response to inhaled corticosteroid therapy in asthma. CRF1 triggers cells to release hormones that are linked to stress and anxiety [original reference missing].Hence CRF1 receptor antagonists are being actively studied as possible treatments for depression and anxiety. Variations in CRHR1 are associated with persistent pulmonary hypertension of the newborn. Corticotropin-releasing hormone receptor 1 has been shown to interact with Corticotropin-releasing hormone and Urocortin. Corticotropin-releasing hormone receptor 1 Corticotropin-releasing hormone receptor 1 (CRHR1) is a protein, also known as CRF, with the latter (CRF) now being the IUPHAR-recommended

neg: Steroid hormone receptor receptors of the nuclear receptor family are all transcription factors. Depending upon the type of receptor, they are either located in the cytosol and move to the cell nucleus upon activation, or remain in the nucleus waiting for the steroid hormone to enter and activate them. This uptake into the nucleus is facilitated by nuclear localization signal (NLS) found in the hinge region of the receptor. This region of the receptor is covered up by heat shock proteins (HSPs) which bind the receptor until the hormone is present. Upon binding by the hormone the receptor undergoes a conformational change releasing

neg: Gonadotropin-releasing hormone antagonist leads to a surge in testosterone or estrogen levels, GnRH antagonists have an immediate onset of action and rapidly reduce sex hormone levels without an initial surge. GnRH antagonists include peptides such as cetrorelix and non-peptide and small-molecule compounds such as elagolix. Peptide GnRH antagonists are GnRH analogues. Gonadotropin-releasing hormone antagonist Gonadotropin-releasing hormone antagonists (GnRH antagonists) are a class of medications that antagonize the gonadotropin-releasing hormone receptor (GnRH receptor) and thus the action of gonadotropin-releasing hormone (GnRH). They are used in the treatment of prostate cancer, endometriosis, uterine fibroids, female infertility in assisted reproduction, and for other indications. Some GnRH

neg: Gonadotropin-releasing hormone antagonist Gonadotropin-releasing hormone antagonist Gonadotropin-releasing hormone antagonists (GnRH antagonists) are a class of medications that antagonize the gonadotropin-releasing hormone receptor (GnRH receptor) and thus the action of gonadotropin-releasing hormone (GnRH). They are used in the treatment of prostate cancer, endometriosis, uterine fibroids, female infertility in assisted reproduction, and for other indications. Some GnRH antagonists, such as cetrorelix, are similar in structure to natural GnRH (a hormone made by neurons in the hypothalamus) but that have an antagonistic effect, while other GnRH antagonists, such as elagolix, are non-peptide and small-molecule compounds. GnRH antagonists compete with natural GnRH for binding to GnRH receptors,

neg: Delta wave during sleep. Delta waves have been shown to be mediated in part by T-type calcium channels. During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA). Delta activity stimulates the release of several hormones, including growth hormone releasing hormone GHRH and prolactin (PRL). GHRH is released from the hypothalamus, which in turn stimulates release of growth hormone (GH) from the pituitary. The secretion of (PRL), which is closely related to (GH), is also regulated by the pituitary. The release of thyroid stimulating hormone (TSH), is decreased in response to delta-wave signaling. Infants have been shown to spend a

neg: Growth hormone–releasing hormone been used in the diagnosis of deficiencies in growth hormone secretion. Tesamorelin, under the trade name Egrifta, received U.S. Food and Drug Administration approval in 2010 for the treatment of lipodystrophy in HIV patients under highly active antiretroviral therapy, and, in 2011, was investigated for effects on certain cognitive tests in the elderly. As a category, the use of GHRH analogs by professional athletes may be prohibited by restrictions on doping in sport because they act as growth hormone secretagogues. Growth hormone–releasing hormone Growth hormone–releasing hormone (GHRH), also known as somatocrinin or by several other names in its endogenous forms

neg: Lactotropic cell Lactotropic cell A lactotropic cell (also known as prolactin cell, epsilon acidophil, lactotrope, lactotroph, mammatroph, mammotroph) is a cell in the anterior pituitary which produces prolactin in response to hormonal signals including dopamine which is inhibitory and thyrotropin-releasing hormone which is stimulatory. Other regulators include oxytocin, estrogen and progesterone. Prolactin is involved in the maturation of mammary glands and their secretion of milk in association with oxytocin, estrogen, progesterone, glucocorticoids, and others. Prolactin has numerous other effects in both sexes. Prolactin cells are acidophilic by hematoxylin & eosin stains and comprise about 20% of all cells in the anterior pituitary

neg: Thyrotropin receptor Thyrotropin receptor The thyrotropin receptor (or TSH receptor) is a receptor (and associated protein) that responds to thyroid-stimulating hormone (also known as "thyrotropin") and stimulates the production of thyroxine (T4) and triiodothyronine (T3). The TSH receptor is a member of the G protein-coupled receptor superfamily of integral membrane proteins and is coupled to the G protein. It is primarily found on the surface of the thyroid epithelial cells, but also found on adipose tissue and fibroblasts. The latter explains the reason of the myxedema finding during Graves disease. Upon binding circulating TSH, a G-protein signal cascade activates adenylyl cyclase and

neg: Growth hormone secretagogue Growth hormone secretagogue Growth hormone secretagogues (GSHs) are a class of drugs which act as secretagogues (i.e., induce the secretion) of growth hormone (GH). They include agonists of the ghrelin/growth hormone secretagogue receptor (GHSR), such as ghrelin (lenomorelin), pralmorelin (GHRP-2), GHRP-6, examorelin (hexarelin), ipamorelin, and ibutamoren (MK-677), and agonists of the growth hormone-releasing hormone receptor (GHRHR), such as growth hormone-releasing hormone (GHRH) (somatorelin), CJC-1295, sermorelin, and tesamorelin. Many also induce the secretion of insulin-like growth factor 1 (IGF-1), as well as of other hypothalamic-pituitary hormones such as prolactin and cortisol. The main clinical application of these agents is the treatment

neg: CJC-1295 CJC-1295 CJC-1295, also known as DAC:GRF (short for drug affinity complex:growth hormone-releasing factor), is a synthetic analogue of growth hormone-releasing hormone (GHRH) (also known as "growth hormone-releasing factor" ("GRF")) and a growth hormone secretagogue (GHS) which was developed by ConjuChem Biotechnologies. It is a modified form of GHRH (1-29) with improved pharmacokinetics, especially in regard to half-life. CJC-1295 markedly increases plasma growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels in both animals and humans. With a single injection, in human subjects, CJC-1295 increases plasma GH levels by 2- to 10-fold for 6 days or longer and plasma IGF-1

neg: Hypothyroidism may include fatigue, cold intolerance, sleepiness, muscle weakness, constipation, a delay in growth, overweight for height, pallor, coarse and thick skin, increased body hair, irregular menstrual cycles in girls, and delayed puberty. Signs may include delayed relaxation of the ankle reflex and a slow heart beat. A goiter may be present with a completely enlarged thyroid gland; sometimes only part of the thyroid is enlarged and it can be knobby in character. Hypothyroidism is caused by inadequate function of the gland itself (primary hypothyroidism), inadequate stimulation by thyroid-stimulating hormone from the pituitary gland (secondary hypothyroidism), or inadequate release of thyrotropin-releasing

neg: Endometrium of these genes are more specifically expressed in the endometrium with only a handful genes being highly endometrium specific. The corresponding specific proteins are expressed in the glandular and stromal cells of the endometrial mucosa. The expression of many of these proteins vary depending on the menstrual cycle, for example the progestorone receptor and thyrotropin-releasing hormone both expressed in the proliferative phase, and PAEP expressed in the secretory phase. Other proteins such as the HOX11 protein that is required for female fertility, is expressed in endometrial stroma cells throughout the menstrual cycle. Certain specific proteins such as the estrogen receptor

neg: Corticotropic cell to the anterior pituitary via the hypophyseal portal system. The adrenocorticotropin hormone stimulates the adrenal cortex to release glucocorticoids and some MSH- (melanocyte stimulating hormone). Stimuli for the release of corticotropin releasing hormones are Glucocorticoids inhibit the release of corticotropin releasing hormone and adrenocorticotropin hormone. Corticotropic cell Corticotropes (or corticotrophs) are basophilic cells in the anterior pituitary that produce melanocyte-stimulating hormone, adrenocorticotropic hormone (ACTH) and lipotropin. The cells produce pro-opiomelanocortin (POMC) which undergoes cleavage to ACTH and β-lipotropin (β-LPH). These cells respond to corticotropin releasing hormone (CRH) and make up about 20% of the cells in the anterior pituitary. Coticotrophs

neg: Prolactin breast, lymphocytes, leukocytes and prostate. Pituitary PRL is controlled by the Pit-1 transcription factor that binds to the prolactin gene at several sites. Ultimately dopamine, extrapituitary PRL is controlled by a superdistal promoter and apparently unaffected by dopamine. The thyrotropin-releasing hormone and the vasoactive intestinal peptide stimulate the secretion of prolactin in experimental settings, however their physiological influence is unclear. The main stimulus for prolactin secretion is suckling, the effect of which is neuronally mediated. A key regulator of prolactin production is estrogens that enhance growth of prolactin-producing cells and stimulate prolactin production directly, as well as suppressing dopamine. In

neg: Hypopituitarism levels confirm a pituitary problem; after the menopause (when LH/FSH levels are normally elevated and the ovaries produce less estradiol), inappropriately low LH/FSH alone is sufficient. Stimulation tests with GnRH are possible, but their use is not encouraged. For TSH, basal measurements are usually sufficient, as well as measurements of thyroxine to ensure that the pituitary is not simply suppressing TSH production in response to hyperthyroidism (an overactive thyroid gland). A stimulation test with thyrotropin-releasing hormone (TRH) is not regarded as useful. Prolactin can be measured by basal level, and is required for the interpretation of LH and FSH results

neg: Thyroid function tests generally increased in hypothyroidism and decreased in hyperthyroidism, making it the most important test for early detection of both of these conditions. The result of this assay is suggestive of the presence and cause of thyroid disease, since a measurement of elevated TSH generally indicates hypothyroidism, while a measurement of low TSH generally indicates hyperthyroidism. However, when TSH is measured by itself, it can yield misleading results, so additional thyroid function tests must be compared with the result of this test for accurate diagnosis. TSH is produced in the pituitary gland. The production of TSH is controlled by thyrotropin-releasing hormone

neg: Lactotropic cell gland. If these cells undergo neoplastic transformation, they will give rise to a prolactinoma, a prolactin-secreting pituitary adenoma. Lactotropic cell A lactotropic cell (also known as prolactin cell, epsilon acidophil, lactotrope, lactotroph, mammatroph, mammotroph) is a cell in the anterior pituitary which produces prolactin in response to hormonal signals including dopamine which is inhibitory and thyrotropin-releasing hormone which is stimulatory. Other regulators include oxytocin, estrogen and progesterone. Prolactin is involved in the maturation of mammary glands and their secretion of milk in association with oxytocin, estrogen, progesterone, glucocorticoids, and others. Prolactin has numerous other effects in both sexes. Prolactin cells

neg: TRH stimulation test is in the anterior pituitary gland, i.e. the pituitary is not secreting TSH. Therefore, even when TRH is given exogenously, TSH levels do not rise as the pituitary is diseased. TRH may cause nausea, vomiting and some patients experience an urge to urinate. Rarely, TRH may cause blood vessel constriction leading to hemorrhage in patients with pre-existing pituitary tumors. Accordingly, patients should be advised about the risks, albeit rare, of TRH testing. 3. http://www.auburn.edu/~deruija/endo_thyroidfts.pdf TRH stimulation test Prior to the availability of sensitive TSH assays, thyrotropin releasing hormone or TRH stimulation tests were relied upon for confirming and assessing the

neg: Growth hormone secretagogue of growth hormone deficiency. They also see black market use, similarly to anabolic steroids, for bodybuilding purposes. Growth hormone secretagogue Growth hormone secretagogues (GSHs) are a class of drugs which act as secretagogues (i.e., induce the secretion) of growth hormone (GH). They include agonists of the ghrelin/growth hormone secretagogue receptor (GHSR), such as ghrelin (lenomorelin), pralmorelin (GHRP-2), GHRP-6, examorelin (hexarelin), ipamorelin, and ibutamoren (MK-677), and agonists of the growth hormone-releasing hormone receptor (GHRHR), such as growth hormone-releasing hormone (GHRH) (somatorelin), CJC-1295, sermorelin, and tesamorelin. Many also induce the secretion of insulin-like growth factor 1 (IGF-1), as well as of other

neg: Pituitary pars intermedia dysfunction have a positive endogenous ACTH test. Horses with early disease may produce a false-negative result. In these horses, the thyrotropin-releasing hormone stimulation test should either be used as an initial screening test, or to confirm a false resting ACTH. Insulin dysregulation is commonly seen in horses with PPID or equine metabolic syndrome, and is associated with obesity. It is of interest primarily because of its link to laminitis. Horses with ID will have an increased insulin response after they are given oral sugars, which will cause a subsequent rise in blood insulin levels, or hyperinsulinemia. Hyperinsulinemia results in decreased tissue

neg: Hypothalamic disease Hypothalamic disease Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, genetic disorders, radiation, surgery, head trauma, lesion, tumour or other physical injury to the hypothalamus. The hypothalamus is the control center for several endocrine functions. Endocrine systems controlled by the hypothalamus are regulated by anti-diuretic hormone (ADH), corticotropin-releasing hormone, gonadotropin-releasing hormone, growth hormone-releasing hormone, oxytocin, all of which are secreted by the hypothalamus. Damage to the hypothalamus may impact any of these hormones and the related endocrine systems. Many of these hypothalamic hormones

neg: Thyrotropin-releasing hormone injection (brand name Relefact TRH) to test the response of the anterior pituitary gland; this procedure is known as a TRH test. This is done as diagnostic test of thyroid disorders such as secondary hypothyroidism and in acromegaly. TRH has anti-depressant and anti-suicidal properties, and in 2012 the U.S. Army awarded a research grant to develop a TRH nasal spray in order to prevent suicide amongst its ranks. TRH has been shown in mice to be an anti-aging agent with a broad spectrum of activities that, because of their actions, suggest that TRH has a fundamental role in the regulation

neg: Growth hormone–releasing hormone the anterior pituitary gland, where it stimulates growth hormone (GH) secretion by stimulating the growth hormone-releasing hormone receptor. GHRH is released in a pulsatile manner, stimulating similar pulsatile release of GH. In addition, GHRH also promotes slow-wave sleep directly. Growth hormone is required for normal postnatal growth, bone growth, regulatory effects on protein, carbohydrate, and lipid metabolism. GHRH stimulates GH production and release by binding to the GHRH Receptor (GHRHR) on cells in the anterior pituitary. The GHRHR is a member of the secretin family of G protein-coupled receptors, and is located on chromosome 7. This protein is transmembranous with

neg: Derek George Smyth human mammary gland and is secreted in the milk. Biochem. Biophys. Acta, 1475, 55-60. 59. Smyth, D.G., del Rio-Garcia, J., Wallnofer, H., Gogl, H., Simma, W., Huber, A., Embacher, R., Fraser, H. and Kreil, G. (1999) Protirelin (thyrotropin-releasing hormone) in the thyroid gland: possible involvement in regulation of thyroid status. Acta Pharmacol. Sin., 20, 289-291. 60. Smyth, D.G. (1997) Discovering biologically active peptides; from structure to function, Anales de la Real Academia de Medicina y Cirugia de Murcia. 49-70. 61. Smyth, D.G. (2016) Lipotropin & beta-endorphin: a Perspective. J. Mol Endocrinol. Derek George Smyth Derek Smyth is a British born

neg: Non-tropic hormone The Hypothalamic-pituitary-adrenal axis is a perfect example of this chain reaction. The reaction begins in the hypothalamus with a release of corticotropin-releasing hormone/factor (CRH/F; tropic). This stimulates the anterior pituitary and causes it to release Adrenocorticotropic hormone (ACTH; tropic) to the adrenal glands. Lastly, cortisol (non-tropic) is secreted from the adrenal glands and goes into the bloodstream where it can have more widespread effects on organs and tissues. Since cortisol is what finally reaches other tissues in the body, it is a non-tropic hormone. CRH an ACTH are tropic hormones because they act on the anterior pituitary gland and adrenal

neg: Modified GRF (1-29) 30 minutes. Modified GRF (1-29) Modified GRF (1-29) often abbreviated as mod GRF (1-29), originally known as tetrasubstitued GRF (1-29), is a term used to identify a 29 amino acid peptide analogue of growth-hormone-releasing hormone (GHRH), a releasing hormone of growth hormone (GH). It is a modified version of the shortest fully functional fragment of GHRH, often referred to as growth hormone releasing factor (1-29) (abbreviated as GRF (1-29)), and also known by its standardized name, sermorelin. The first 29 amino acids of GHRH were discovered to be as equally potent as its full 44 amino acid structure This fragment

neg: Modified GRF (1-29) Modified GRF (1-29) Modified GRF (1-29) often abbreviated as mod GRF (1-29), originally known as tetrasubstitued GRF (1-29), is a term used to identify a 29 amino acid peptide analogue of growth-hormone-releasing hormone (GHRH), a releasing hormone of growth hormone (GH). It is a modified version of the shortest fully functional fragment of GHRH, often referred to as growth hormone releasing factor (1-29) (abbreviated as GRF (1-29)), and also known by its standardized name, sermorelin. The first 29 amino acids of GHRH were discovered to be as equally potent as its full 44 amino acid structure This fragment became known