Pituitary Gland, Anterior
Thyrotropin, beta Subunit
Thyrotropin
Thyrotropin-Releasing Hormone
Pituitary Gland
Antithyroid Agents
Thyroxine
Intracellular gonadotropin-releasing hormone receptors in breast cancer and gonadotrope lineage cells. (1/18)
Gonadotropin-releasing hormone receptors (GnRHRs) are expressed in gonadotropes and several extra-pituitary sites. They are assumed to be cell surface proteins but the human (h) GnRHR lacks features favoring plasma membrane localization and receptor location varies with cell type. When expressed in mammary (MCF7) cells, cell surface hGnRHR binding was much lower than that of mouse and sheep GnRHRs (type I GnRHRs without C-terminal tails), Xenopus (X) and marmoset type II GnRHRs (type II GnRHRs with C-tails) or chimeric receptors (type I GnRHRs with added XGnRHR C-tails). hGnRHR binding was higher in alphaT4 (gonadotrope-derived) cells and was increased less by C-tail addition. Whole cell levels of tagged human, Xenopus and chimeric GnRHRs were comparable (Western blotting) and confocal microscopy revealed that the hGnRHR is primarily intracellular (distribution similar to the endoplasmic reticulum marker, calreticulin), whereas most XGnRHR is at the plasma membrane, and adding the C-tail increased cell surface hGnRHR levels. A membrane-permeant antagonist increased cell surface hGnRHR number (>4-fold, t1/2 = 4 h) and also increased hGnRHR signaling and hGnRHR-mediated inhibition of proliferation. A more rapid increase in hGnRHR binding occurred when the temperature was raised from 4 to 37 degrees C (>5-fold, t1/2 = 15 min) and this effect was prevented by mutation to prevent signaling. Thus, cell surface GnRHR expression depends on receptor and cell type and the hGnRHR is primarily an intracellular protein that traffics to the cell surface for signaling in MCF7 cells. Manipulations favoring such trafficking may facilitate selective targeting of extra-pituitary GnRHRs. (+info)Cell-specific expression of X-linked inhibitor of apoptosis in the anterior pituitary of streptozotocin-induced diabetic rats. (2/18)
Cell death is increased in the anterior pituitary of poorly controlled diabetic rats, but anti-apoptotic mechanisms are also activated. We hypothesized that specific cell types are selectively protected against diabetes-induced cell death. To determine when anti-apoptotic mechanisms are activated, streptozotocin-induced diabetic rats were killed after 1, 4, 6 and 8 weeks of evolution. Anterior pituitaries were processed for western blot analysis to determine changes in the intrinsic cell death pathway and upstream kinases involved in cell protection mechanisms. An increase in cell death was detected by ELISA at 4 weeks of diabetes. TUNEL labelling demonstrated that this corresponded to death of primarily lactotrophs, a few somatotrophs, and no thyrotrophs, corticotrophs or gonadotrophs. Levels of phosphorylated (p) Akt were increased at 1 week of diabetes, while pERK1/2 levels increased at 4 weeks and pJNK at 6 weeks. Activation of caspase 3 decreased and anti-apoptotic members of the Bcl-2 protein family increased as early as 1 week after diabetes onset. These changes were coincident with increased IGF-I receptor levels. Levels of X-linked inhibitor of apoptosis protein (XIAP) increased significantly after 6 weeks of diabetes, as did activation of nuclear factor (NF)kappaB. Double immunohistochemistry indicated that XIAP was expressed in less than 1% of lactotrophs and gonadotrophs, approximately 50% of somatotrophs and more than 90% of corticotrophs and thyrotrophs. These results suggest that some cell survival mechanisms are rapidly activated in the anterior pituitary, even before increased cell death can be detected, while others are more delayed. Furthermore, both pituitary cell death and expression of protective mechanisms such as XIAP are cell-type specific. (+info)Hes1 is required for pituitary growth and melanotrope specification. (3/18)
Rathke's pouch contains progenitor cells that differentiate into the endocrine cells of the pituitary gland. It gives rise to gonadotrope, thyrotrope, somatotrope, corticotrope and lactotrope cells in the anterior lobe and the intermediate lobe melanotropes. Pituitary precursor cells express many members of the Notch signaling pathway including the downstream effector gene Hes1. We hypothesized that Hes1 regulates the timing of precursor differentiation and cell fate determination. To test this idea, we expressed Hes1 in differentiating pituitary cells and found that it can inhibit gonadotrope and thyrotrope differentiation. Pituitaries of Hes1 deficient mice have anterior lobe hypoplasia. All cells in the anterior lobe are specified and differentiate, but an early period of increased cell death and reduced proliferation causes reduced growth, evident as early as e14.5. In addition, cells within the intermediate lobe differentiate into somatotropes instead of melanotropes. Thus, the Hes1 repressor is essential for melanotrope specification. These results demonstrate that Notch signaling plays multiple roles in pituitary development, influencing precursor number, organ size, cell differentiation and ultimately cell fate. (+info)Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. (4/18)
TSH-secreting adenoma is a rare pituitary adenoma, and the expression levels of the specific subtypes of somatostatin receptors (sstr) mRNAs have remained obscure. To determine the quantitative expression of the sstr1-5 mRNAs in TSH-secreting adenomas that may be related to the efficacy of treatment with a somatostatin analogue, expression of the sstr1-5 mRNAs was examined and compared in TSH-secreting adenomas and other pituitary adenomas. The pituitary adenomas were obtained at transsphenoidal surgery from 4 cases of TSH-secreting adenoma, including 1 patient showing a significant shrinkage of the tumor size after only 10 days of octreotide treatment, 2 patients without tumor size reduction and 1 patient without treatment, and 5 GH-secreting adenomas, 6 prolactinomas, 5 nonfunctioning adenomas, 4 ACTH-secreting adenomas and normal pituitaries at autopsy from 4 normal subjects. In comparison to the normal pituitary, sstr2A>sstr1>sstr5>sstr3 mRNAs were expressed in the TSH-secreting adenomas examined. No expression of sstr2B or sstr4 mRNA was observed. The expression level of sstr2 mRNA was significantly higher than those in normal pituitary, prolactinomas, ACTH-secreting and nonfunctioning pituitary adenomas. The patient with marked shrinkage of the tumor showed the highest expression of both sstr2 and sstr5 mRNAs among all the cases of pituitary adenoma. A TSH-secreting tumor without shrinkage showed a similar expression level of sstr2 mRNA. These findings demonstrated that TSH-secreting adenomas express sstr1, 2A, 3 and 5 mRNAs, predominantly sstr2A, and in addition to the expression of sstr2 mRNA, the expression level of sstr5 mRNA may be a factor affecting the tumor shrinkage by somatostatin analogues against TSH-secreting adenomas. (+info)Hypothalamic input is required for development of normal numbers of thyrotrophs and gonadotrophs, but not other anterior pituitary cells in late gestation sheep. (5/18)
To evaluate the hypothalamic contribution to the development of anterior pituitary (AP) cells we surgically disconnected the hypothalamus from the pituitary (hypothalamo-pituitary disconnection, HPD) in fetal sheep and collected pituitaries 31 days later. Pituitaries (n = 6 per group) were obtained from fetal sheep (term = 147 +/- 3 days) at 110 days (unoperated group) of gestation and at 141 days from animals that had undergone HPD or sham surgery at 110 days. Cells were identified by labelling pituitary sections with antisera against the six AP hormones. Additionally, we investigated the colocalization of glycoprotein hormones. The proportions of somatotrophs and corticotrophs were unchanged by age or HPD. Lactotrophs increased 80% over time, but the proportion was unaffected by HPD. Thyrotrophs, which were unaffected by age, increased 70% following HPD. Gonadotrophs increased with gestational age (LH+ cells 55%; FSH+ cells 19-fold), but this was severely attenuated by HPD. We investigated the possible existence of a reciprocal effect of HPD on multipotential glycoprotein-expressing cells. Co-expression of LH and TSH was extremely rare (< 1%) and unchanged over the last month of gestation or HPD. The increase of gonadotrophs expressing FSH only or LH and FSH was attenuated by HPD. Therefore, the proportions of somatotrophs, lactotrophs and corticotrophs are regulated independently of hypothalamic input in the late gestation fetal pituitary. In marked contrast, the determination of the thyrotroph and gonadotroph lineages over the same time period is subject to complex mechanisms involving hypothalamic factors, which inhibit differentiation and/or proliferation of thyrotrophs, but stimulate gonadotrophs down the FSH lineage. Development of a distinct population of gonadotrophs, expressing only LH, appears to be subject to alternative mechanisms. (+info)Immunohistochemical and morphometric study of pituitary pars distalis thyrotrophs of male viscacha (Lagostomus maximus maximus): seasonal variations and effect of melatonin and castration. (6/18)
(+info)Immunohistochemical distribution of regulatory peptides in the human fetal adenohypophysis. (7/18)
(+info)Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog. (8/18)
Pituitary thyrotroph hyperplasia results from prolonged primary hypothyroidism in humans, mice and rats. In dogs with Cushing's disease, many cases have low serum thyroid hormones concentrations due to euthyroid sick syndrome. A 6-year-old castrated male Beagle diagnosed with Cushing's disease had a high serum thyroid stimulating hormone (TSH) concentration that was treated by hypophysectomy. On histological examination, the resected pituitary gland contained both a corticotroph adenoma and thyrotroph hyperplasia. The TSH-positive cell ratio in this case was greater than that of healthy Beagles. In the present case, the pituitary thyrotroph hyperplasia was probably caused by primary hypothyroidism. In conclusion, this Beagle is the first histological confirmation of the coexistence of a corticotroph adenoma and thyrotroph hyperplasia. (+info)Thyrotrophs, also known as thyroid-stimulating hormone (TSH) producing cells, are a type of endocrine cell located in the anterior pituitary gland. They synthesize and secrete TSH, which is a hormone that regulates the function of the thyroid gland by stimulating the production and release of thyroxine (T4) and triiodothyronine (T3), two important thyroid hormones. Thyrotrophs respond to the levels of thyroid hormones in the blood through a negative feedback mechanism, increasing or decreasing TSH secretion as needed to maintain proper levels of T4 and T3.
Sulfadimethoxine is an antimicrobial agent, specifically a sulfonamide. It is defined as a synthetic antibacterial drug that contains the sulfanilamide nucleus and is used to treat various bacterial infections in both humans and animals. In human medicine, it is used to treat urinary tract infections, bronchitis, and traveler's diarrhea. In veterinary medicine, it is commonly used to treat coccidiosis in animals such as poultry, cattle, and pets.
The drug works by inhibiting the bacterial synthesis of folic acid, which is essential for bacterial growth. It is usually administered orally and is available in various forms, including tablets, capsules, and powder for suspension. As with any medication, it should be used under the guidance of a healthcare professional to ensure its safe and effective use.
The anterior pituitary, also known as the adenohypophysis, is the front portion of the pituitary gland. It is responsible for producing and secreting several important hormones that regulate various bodily functions. These hormones include:
* Growth hormone (GH), which stimulates growth and cell reproduction in bones and other tissues.
* Thyroid-stimulating hormone (TSH), which regulates the production of thyroid hormones by the thyroid gland.
* Adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce cortisol and other steroid hormones.
* Follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which regulate reproductive function in both males and females by controlling the development and release of eggs or sperm.
* Prolactin, which stimulates milk production in pregnant and nursing women.
* Melanocyte-stimulating hormone (MSH), which regulates skin pigmentation and appetite.
The anterior pituitary gland is controlled by the hypothalamus, a small region of the brain located just above it. The hypothalamus produces releasing and inhibiting hormones that regulate the secretion of hormones from the anterior pituitary. These hormones are released into a network of blood vessels called the portal system, which carries them directly to the anterior pituitary gland.
Damage or disease of the anterior pituitary can lead to hormonal imbalances and various medical conditions, such as growth disorders, thyroid dysfunction, adrenal insufficiency, reproductive problems, and diabetes insipidus.
Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a hormone produced and released by the anterior pituitary gland. It plays a crucial role in regulating the function of the thyroid gland by stimulating the production and release of thyroid hormones, triiodothyronine (T3) and thyroxine (T4).
The TSH molecule is composed of two subunits: alpha and beta. The alpha subunit is common to several pituitary hormones, including TSH, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and human chorionic gonadotropin (hCG). In contrast, the beta subunit is unique to each hormone, determining its specific biological activity.
Therefore, 'Thyrotropin, beta Subunit' refers to the distinct portion of the TSH molecule that confers its thyroid-stimulating properties and allows it to be identified and measured separately from other pituitary hormones sharing the common alpha subunit. Beta-subunit assays are sometimes used in clinical settings to evaluate thyroid function, as they can provide information about TSH levels independent of the common alpha subunit.
Somatotrophs are a type of cell found within the anterior pituitary gland, a small endocrine gland located at the base of the brain. These cells are responsible for producing and secreting the hormone known as somatotropin or growth hormone (GH). This hormone plays a crucial role in regulating growth, cell reproduction, and regeneration. It also helps to regulate the body's metabolism and maintain proper body composition by promoting the breakdown of fats and the synthesis of proteins. Disorders related to somatotrophs can lead to conditions such as gigantism or dwarfism, depending on whether there is an overproduction or underproduction of growth hormone.
Corticotrophs are a type of endocrine cell found in the anterior pituitary gland. They are responsible for producing and secreting adrenocorticotropic hormone (ACTH), which regulates the function of the adrenal gland. ACTH stimulates the production and release of cortisol, a steroid hormone that helps regulate metabolism, immune response, and stress response among other functions. Corticotrophs are controlled by the hypothalamus through the release of corticotropin-releasing hormone (CRH) and vasopressin. Dysfunction of corticotrophs can lead to various endocrine disorders, such as Cushing's disease, which is characterized by excessive production of ACTH and cortisol.
Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a hormone secreted by the anterior pituitary gland. Its primary function is to regulate the production and release of thyroxine (T4) and triiodothyronine (T3) hormones from the thyroid gland. Thyrotropin binds to receptors on the surface of thyroid follicular cells, stimulating the uptake of iodide and the synthesis and release of T4 and T3. The secretion of thyrotropin is controlled by the hypothalamic-pituitary-thyroid axis: thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release of thyrotropin, while T3 and T4 inhibit its release through a negative feedback mechanism.
Thyrotropin-Releasing Hormone (TRH) is a tripeptide hormone that is produced and released by the hypothalamus in the brain. Its main function is to regulate the release of thyroid-stimulating hormone (TSH) from the anterior pituitary gland. TRH acts on the pituitary gland to stimulate the synthesis and secretion of TSH, which then stimulates the thyroid gland to produce and release thyroid hormones (triiodothyronine (T3) and thyroxine (T4)) into the bloodstream.
TRH is a tripeptide amino acid sequence with the structure of pGlu-His-Pro-NH2, and it is synthesized as a larger precursor molecule called preprothyrotropin-releasing hormone (preproTRH) in the hypothalamus. PreproTRH undergoes post-translational processing to produce TRH, which is then stored in secretory vesicles and released into the hypophyseal portal system, where it travels to the anterior pituitary gland and binds to TRH receptors on thyrotroph cells.
In addition to its role in regulating TSH release, TRH has been shown to have other physiological functions, including modulation of feeding behavior, body temperature, and neurotransmitter release. Dysregulation of the TRH-TSH axis can lead to various thyroid disorders, such as hypothyroidism or hyperthyroidism.
The pituitary gland is a small, endocrine gland located at the base of the brain, in the sella turcica of the sphenoid bone. It is often called the "master gland" because it controls other glands and makes the hormones that trigger many body functions. The pituitary gland measures about 0.5 cm in height and 1 cm in width, and it weighs approximately 0.5 grams.
The pituitary gland is divided into two main parts: the anterior lobe (adenohypophysis) and the posterior lobe (neurohypophysis). The anterior lobe is further divided into three zones: the pars distalis, pars intermedia, and pars tuberalis. Each part of the pituitary gland has distinct functions and produces different hormones.
The anterior pituitary gland produces and releases several important hormones, including:
* Growth hormone (GH), which regulates growth and development in children and helps maintain muscle mass and bone strength in adults.
* Thyroid-stimulating hormone (TSH), which controls the production of thyroid hormones by the thyroid gland.
* Adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce cortisol and other steroid hormones.
* Follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which regulate reproductive function in both males and females.
* Prolactin, which stimulates milk production in pregnant and lactating women.
The posterior pituitary gland stores and releases two hormones that are produced by the hypothalamus:
* Antidiuretic hormone (ADH), which helps regulate water balance in the body by controlling urine production.
* Oxytocin, which stimulates uterine contractions during childbirth and milk release during breastfeeding.
Overall, the pituitary gland plays a critical role in maintaining homeostasis and regulating various bodily functions, including growth, development, metabolism, and reproductive function.
Antithyroid agents are a class of medications that are used to treat hyperthyroidism, a condition in which the thyroid gland produces too much thyroid hormone. These medications work by inhibiting the production of thyroid hormones in the thyroid gland. There are several types of antithyroid agents available, including:
1. Propylthiouracil (PTU): This medication works by blocking the enzyme that is needed to produce thyroid hormones. It also reduces the conversion of thyroxine (T4) to triiodothyronine (T3), another thyroid hormone, in peripheral tissues.
2. Methimazole: This medication works similarly to propylthiouracil by blocking the enzyme that is needed to produce thyroid hormones. However, it does not affect the conversion of T4 to T3 in peripheral tissues.
3. Carbimazole: This medication is converted to methimazole in the body and works similarly to block the production of thyroid hormones.
Antithyroid agents are usually taken orally, and their effects on thyroid hormone production begin within a few hours after ingestion. However, it may take several weeks for patients to notice an improvement in their symptoms. These medications can have side effects, including rash, hives, and joint pain. In rare cases, they can cause liver damage or agranulocytosis, a condition in which the body does not produce enough white blood cells.
It is important to note that antithyroid agents do not cure hyperthyroidism; they only treat the symptoms by reducing thyroid hormone production. Therefore, patients may need to take these medications for several months or even years, depending on their individual circumstances. In some cases, surgery or radioactive iodine therapy may be recommended as alternative treatments for hyperthyroidism.
Thyroxine (T4) is a type of hormone produced and released by the thyroid gland, a small butterfly-shaped endocrine gland located in the front of your neck. It is one of two major hormones produced by the thyroid gland, with the other being triiodothyronine (T3).
Thyroxine plays a crucial role in regulating various metabolic processes in the body, including growth, development, and energy expenditure. Specifically, T4 helps to control the rate at which your body burns calories for energy, regulates protein, fat, and carbohydrate metabolism, and influences the body's sensitivity to other hormones.
T4 is produced by combining iodine and tyrosine, an amino acid found in many foods. Once produced, T4 circulates in the bloodstream and gets converted into its active form, T3, in various tissues throughout the body. Thyroxine has a longer half-life than T3, which means it remains active in the body for a more extended period.
Abnormal levels of thyroxine can lead to various medical conditions, such as hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). These conditions can cause a range of symptoms, including weight gain or loss, fatigue, mood changes, and changes in heart rate and blood pressure.