Pituitary Gland, Anterior
Growth Hormone
Growth Hormone-Releasing Hormone
Pituitary Gland
Gigantism
Somatostatin
Prolactin
Transcription Factor Pit-1
Hyperprolactinemia
Thyrotropin-Releasing Hormone
Molting
Acromegaly
Receptors, Pituitary Hormone-Regulating Hormone
Pituitary Neoplasms
Nifedipine
Immunohistochemistry
Cells, Cultured
Membrane Potentials
Rats, Sprague-Dawley
Immunoenzyme Techniques
Patch-Clamp Techniques
Calcium
Rats, Inbred Strains
Cyclic AMP
Reverse Transcriptase Polymerase Chain Reaction
Human Growth Hormone
Research
Receptors, Somatotropin
Hormones
Cortistatin mimics somatostatin by inducing a dual, dose-dependent stimulatory and inhibitory effect on growth hormone secretion in somatotropes. (1/57)
Cortistatin is a recently discovered neuropeptide that is structurally related to somatostatin, the classic inhibitor of growth hormone (GH) release. Cortistatin binds with high affinity to all five somatostatin receptors (sst1-5), and, like somatostatin, cortistatin inhibits in vivo GH release in man and rats. In this report, we compared the in vitro actions of cortistatin and somatostatin using primary pig pituitary cell cultures. In this species, we have previously reported that somatostatin not only inhibits GH-releasing hormone (GHRH)-stimulated GH release at high doses, but also stimulates basal GH release at low (pM) doses, a dual response that is markedly dependent on the subpopulation of pituitary somatotropes examined. Results reported herein demonstrate that cortistatin closely mimics the dose-dependent inhibitory and stimulatory effects of somatostatin on GH secretion. As cortistatin, unlike somatostatin, binds to the human receptor for ghrelin/GH secretagogs (GHS-R), we also investigated whether cortistatin stimulates GH release through this receptor by using a synthetic, short form of cortistatin, cortistatin-8 (CST8), which lacks the sst-binding capacity of full-length cortistatin but retains its GHS-R-binding capacity. Interestingly, CST8 stimulated GH release only at low doses (10(-15) M), and did not reduce GH secretion stimulated by GHRH, ghrelin, or low-dose, full-length cortistatin, yet it counteracted that induced by a nonpeptidyl GHS, L-163 255. Taken together, our results indicate that the dual, inhibitory and stimulatory effects of cortistatin on GH release closely parallel those of somatostatin and are probably mediated by the same receptor(s) and signaling pathway(s) for both peptides. Furthermore, they suggest that the pathway(s) activated by cortistatin (and somatostatin) to stimulate GH release are not initiated by GHS-R activation. (+info)Examination of the direct effects of metabolic factors on somatotrope function in a non-human primate model, Papio anubis. (2/57)
In humans, circulating GH levels are increased in catabolic states and suppressed in obesity. In both extremes, normalization of the metabolic environment normalizes GH release, leading to the conclusion that changes in metabolic hormones and/or metabolites promote changes in GH synthesis and release. Metabolic regulation of GH secretion can be mediated centrally by modulation of hypothalamic GHRH and somatostatin input to the pituitary and/or by direct regulation of pituitary somatotrope function. Although data are available showing glucocorticoids, free fatty acids (FFA), IGF-I, and insulin have direct effects on rat somatotrope function, little information is available regarding the direct pituitary effects of these metabolic factors in primates. Therefore, this study examined the effects of glucocorticoids (dexamethasone (0.1-100 nM) and hydrocortisone (10 nM)), FFA (oleic and linoleic acid, 100 and 400 microM each), IGF-I (0.5-50 nM), and insulin (0.5-50 nM) on GH release and GH, GHRH-receptor (GHRH-R) and ghrelin-receptor (GHS-R) mRNA levels, in primary pituitary cell cultures of baboons (Papio anubis) after 24 h treatment. A commercial ELISA kit was used to determine the amount of GH released into the media, while quantitative real-time reverse transcription-PCR was used to determine mRNA levels. To design species-specific primers for baboon GH, GHRH-R, GHS-R, insulin receptor (INSR), IGF-I receptor (IGF-IR), pituitary-specific transcription factor-1 (Pit-1), and cyclophilin A (used as a housekeeping gene) cDNA, sequence data for each baboon transcript were obtained and this data were submitted to Genbank. Glucocorticoids, FFA, insulin and IGF-I treatment did not significantly alter the expression of Pit-1, a transcription factor essential for normal somatotrope development and function. However, as previously reported in the rat, glucocorticoids increased, while FFA, IGF-I and insulin decreased GH release in baboon pituitary cell cultures, where changes in GH release were reflected by comparable changes in GH mRNA levels. In addition, glucocorticoids increased, while FFA, IGF-I and insulin decreased the expression of the GH stimulatory receptors, GHRH-R and GHS-R, without significantly altering cyclophilin A mRNA levels. A role of insulin/INSR pathway, independent of IGF-I, in regulating pituitary function is supported by the fact that (1) IGF-I and insulin significantly suppressed somatotrope function at doses (0.5 and 5 nM respectively) not anticipated to activate their respective receptors, and (2) the baboon pituitary expresses INSR mRNA at levels comparable to or greater than that of tissues commonly considered as insulin sensitive (i.e. liver, skeletal muscle, and fat). Taken together, these results demonstrate that metabolic factors can directly modulate primate somatotrope function through regulating GH synthesis and release, as well as mediating the expression of receptors important in central (GHRH) and systemic (ghrelin) regulation of GH secretion. (+info)Localization of vascular endothelial growth factor (VEGF) receptors in normal and adenomatous pituitaries: detection of a non-endothelial function of VEGF in pituitary tumours. (3/57)
As for any solid tumour, pituitary adenoma expansion is dependent on neovascularization through angiogenesis. In this process, vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, VEGFR-2 and neuropilin-1 (NRP-1) may play an outstanding role. The intention of this work was to study the expression/localization and possible function of VEGF receptors in pituitary adenomas. VEGF receptor mRNA and protein expression was studied by in situ hybridization, immunohistochemistry and RT-PCR in 6 normal human pituitaries, 39 human pituitary adenomas and 4 rodent pituitary adenoma cell lines. VEGFR-1 expressing somatotroph MtT-S cells were used as a model to study the role of VEGF on cell proliferation and to elucidate the underlying mechanism of action. In normal pituitaries, VEGFR-1 was detected in endocrine cells, whereas VEGFR-2 and NRP-1 were exclusively expressed in endothelial cells. In pituitary tumours, a heterogeneous VEGFR expression pattern was observed by IHC. VEGFR-1, VEGFR-2 and NRP-1 were detected in 24, 18 and 17 adenomas respectively. In the adenomas, VEGFR-1 was expressed in epithelial tumour cells and VEGFR-2/NRP-1 in vessel endothelial cells. Functional studies in VEGFR-1-positive MtT-S cells showed that the ligands of VEGFR-1 significantly stimulated cell proliferation. This effect was mediated through the phosphatidylinositol-3-kinase-signalling pathway and involves induction of cyclin D1 and Bcl-2. Based on our results, we speculate that the ligands of VEGF receptors, such as VEGF-A and placenta growth factor, not only play a role in angiogenesis in pituitary adenomas, but also affect the growth of pituitary tumour cells through VEGFR-1. (+info)The rate of c-fos transcription in vivo is continuously regulated at the level of elongation by dynamic stimulus-coupled recruitment of positive transcription elongation factor b. (4/57)
In mammalian cells, multiple stimuli induce the expression of the immediate early gene c-fos. The specificity of c-fos transcriptional response depends on the activation of signaling protein kinases, transcription factors, and chromatin-modifying complexes but also on a regulated block to elongation in the first intron. Here we show by chromatin immunoprecipitation that finely tuned control of c-fos gene expression by distinct stimuli is associated with a dynamic regulation of transcription elongation and differential phosphorylation of the C-terminal domain of RNA polymerase II. Comparison of two stimuli of c-fos expression in the pituitary cell line GH4C1, namely the thyrotropin-releasing hormone versus depolarizing KCl, shows that both stimuli increase initiation, but only thyrotropin-releasing hormone is efficient to stimulate elongation and thus produce high transcription rates. To control elongation, the elongation factor P-TEFb is recruited to the 5'-end of the gene in a stimuli and time-dependent manner. Transition from initiation to elongation depends also on the dynamic recruitment of the initiation factors TFIIB and TFIIE but not TFIID, which remains constitutively bound on the promoter. It thus appears that tight coupling of signaling input to transcriptional output rate is achieved by c-fos gene-specific mechanisms, which control post-initiation steps rather than pre-initiation complex assembly. (+info)Adaptive stress response in segmental progeria resembles long-lived dwarfism and calorie restriction in mice. (5/57)
How congenital defects causing genome instability can result in the pleiotropic symptoms reminiscent of aging but in a segmental and accelerated fashion remains largely unknown. Most segmental progerias are associated with accelerated fibroblast senescence, suggesting that cellular senescence is a likely contributing mechanism. Contrary to expectations, neither accelerated senescence nor acute oxidative stress hypersensitivity was detected in primary fibroblast or erythroblast cultures from multiple progeroid mouse models for defects in the nucleotide excision DNA repair pathway, which share premature aging features including postnatal growth retardation, cerebellar ataxia, and death before weaning. Instead, we report a prominent phenotypic overlap with long-lived dwarfism and calorie restriction during postnatal development (2 wk of age), including reduced size, reduced body temperature, hypoglycemia, and perturbation of the growth hormone/insulin-like growth factor 1 neuroendocrine axis. These symptoms were also present at 2 wk of age in a novel progeroid nucleotide excision repair-deficient mouse model (XPD(G602D/R722W)/XPA(-/-)) that survived weaning with high penetrance. However, despite persistent cachectic dwarfism, blood glucose and serum insulin-like growth factor 1 levels returned to normal by 10 wk, with hypoglycemia reappearing near premature death at 5 mo of age. These data strongly suggest changes in energy metabolism as part of an adaptive response during the stressful period of postnatal growth. Interestingly, a similar perturbation of the postnatal growth axis was not detected in another progeroid mouse model, the double-strand DNA break repair deficient Ku80(-/-) mouse. Specific (but not all) types of genome instability may thus engage a conserved response to stress that evolved to cope with environmental pressures such as food shortage. (+info)Characterisation of the mouse vasoactive intestinal peptide receptor type 2 gene, Vipr2, and identification of a polymorphic LINE-1-like sequence that confers altered promoter activity. (6/57)
The VPAC(2) receptor is a seven transmembrane spanning G protein-coupled receptor for two neuropeptides, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP). It has a distinct tissue-specific, developmental and inducible expression that underlies an important neuroendocrine role. Here, we report the characterisation of the gene that encodes the mouse VPAC(2) receptor (Vipr2), localisation of the transcriptional start site and functional analysis of the promoter region. The Vipr2 gene contains 12 introns within its protein-coding region and spans 68.6 kb. Comparison of the 5' untranslated region sequences for cloned 5'-RACE products amplified from different tissues showed they all were contained within the same exon, with the longest extending 111 bp upstream of the ATG start site. Functional analysis of the 3.2-kb 5'-flanking region using sequentially deleted sequences cloned into a luciferase gene reporter vector revealed that this region is active as a promoter in mouse AtT20 D16:16 and rat GH4C1 cell lines. The core promoter is located within a 180-bp GC-rich region proximal to the ATG start codon and contains potential binding sites for Sp1 and AP2, but no TATA-box. Further upstream, in two out of three mice strains examined, we have discovered a 496-bp polymorphic DNA sequence that bears a significant identity to mouse LINE-1 DNA. Comparison of the promoter activity between luciferase reporter gene constructs derived from the BALB/c (which contains this sequence) and C57BL/6J (which lacks this sequence) Vipr2 promoter regions has shown three-fold difference in luciferase gene activity when expressed in mouse AtT20 D16:16 and alphaT3-1 cells, but not when expressed in the rat GH4C1 cells or in COS 7 cells. Our results suggest that the mouse Vipr2 gene may be differentially active in different mouse strains, depending on the presence of this LINE-1-like sequence in the promoter region. (+info)Cell-specific expression of X-linked inhibitor of apoptosis in the anterior pituitary of streptozotocin-induced diabetic rats. (7/57)
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)Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome. (8/57)
Cockayne syndrome (CS) is a photosensitive, DNA repair disorder associated with progeria that is caused by a defect in the transcription-coupled repair subpathway of nucleotide excision repair (NER). Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis. (+info)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.
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.
Growth Hormone (GH), also known as somatotropin, is a peptide hormone secreted by the somatotroph cells in the anterior pituitary gland. It plays a crucial role in regulating growth, cell reproduction, and regeneration by stimulating the production of another hormone called insulin-like growth factor 1 (IGF-1) in the liver and other tissues. GH also has important metabolic functions, such as increasing glucose levels, enhancing protein synthesis, and reducing fat storage. Its secretion is regulated by two hypothalamic hormones: growth hormone-releasing hormone (GHRH), which stimulates its release, and somatostatin (SRIF), which inhibits its release. Abnormal levels of GH can lead to various medical conditions, such as dwarfism or gigantism if there are deficiencies or excesses, respectively.
Growth Hormone-Releasing Hormone (GHRH) is a hormone that is produced and released by the hypothalamus, a small gland located in the brain. Its primary function is to stimulate the anterior pituitary gland to release growth hormone (GH) into the bloodstream. GH plays a crucial role in growth and development, particularly during childhood and adolescence, by promoting the growth of bones and muscles.
GHRH is a 44-amino acid peptide that binds to specific receptors on the surface of pituitary cells, triggering a series of intracellular signals that ultimately lead to the release of GH. The production and release of GHRH are regulated by various factors, including sleep, stress, exercise, and nutrition.
Abnormalities in the production or function of GHRH can lead to growth disorders, such as dwarfism or gigantism, as well as other hormonal imbalances. Therefore, understanding the role of GHRH in regulating GH release is essential for diagnosing and treating these conditions.
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.
Lactotrophs, also known as mammotrophs or prolactin cells, are a type of hormone-producing cell found in the anterior pituitary gland. They are responsible for producing and secreting the hormone prolactin, which plays a crucial role in lactation (milk production) in females after childbirth. Prolactin also has other functions in the body, such as regulating immune responses, metabolism, and behavior. Lactotrophs can be stimulated by factors like estrogen, thyroid-stimulating hormone (TSH), and stress, leading to increased prolactin secretion.
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.
Gigantism is a rare medical condition characterized by excessive growth and height significantly above average. This occurs due to an overproduction of growth hormone (GH), also known as somatotropin, during the growth phase in childhood. The pituitary gland, a small gland located at the base of the brain, is responsible for producing this hormone.
In gigantism, the pituitary gland releases too much GH, leading to abnormal bone and tissue growth. This condition is different from acromegaly, which is characterized by excessive GH production in adulthood after the growth phase has ended. In both cases, the excess GH can lead to various health complications, including cardiovascular disease, diabetes, hypertension, and joint problems.
Gigantism is typically caused by a benign tumor called a pituitary adenoma that presses against and stimulates the production of GH from the anterior pituitary gland. Treatment usually involves surgical removal of the tumor or medication to control GH levels, depending on the severity and progression of the condition. Early diagnosis and treatment are crucial for managing the symptoms and preventing long-term health complications associated with gigantism.
Somatostatin is a hormone that inhibits the release of several hormones and also has a role in slowing down digestion. It is produced by the body in various parts of the body, including the hypothalamus (a part of the brain), the pancreas, and the gastrointestinal tract.
Somatostatin exists in two forms: somatostatin-14 and somatostatin-28, which differ in their length. Somatostatin-14 is the predominant form found in the brain, while somatostatin-28 is the major form found in the gastrointestinal tract.
Somatostatin has a wide range of effects on various physiological processes, including:
* Inhibiting the release of several hormones such as growth hormone, insulin, glucagon, and gastrin
* Slowing down digestion by inhibiting the release of digestive enzymes from the pancreas and reducing blood flow to the gastrointestinal tract
* Regulating neurotransmission in the brain
Somatostatin is used clinically as a diagnostic tool for detecting certain types of tumors that overproduce growth hormone or other hormones, and it is also used as a treatment for some conditions such as acromegaly (a condition characterized by excessive growth hormone production) and gastrointestinal disorders.
Prolactin is a hormone produced by the pituitary gland, a small gland located at the base of the brain. Its primary function is to stimulate milk production in women after childbirth, a process known as lactation. However, prolactin also plays other roles in the body, including regulating immune responses, metabolism, and behavior. In men, prolactin helps maintain the sexual glands and contributes to paternal behaviors.
Prolactin levels are usually low in both men and non-pregnant women but increase significantly during pregnancy and after childbirth. Various factors can affect prolactin levels, including stress, sleep, exercise, and certain medications. High prolactin levels can lead to medical conditions such as amenorrhea (absence of menstruation), galactorrhea (spontaneous milk production not related to childbirth), infertility, and reduced sexual desire in both men and women.
Transcription Factor Pit-1, also known as POU1F1 or pituitary-specific transcription factor 1, is a protein that plays a crucial role in the development and function of the anterior pituitary gland. It is a member of the POU domain family of transcription factors, which are characterized by a conserved DNA-binding domain.
Pit-1 is essential for the differentiation and proliferation of certain types of pituitary cells, including those that produce growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH). Pit-1 binds to specific DNA sequences in the promoter regions of these hormone genes, thereby activating their transcription and promoting hormone production.
Mutations in the gene encoding Pit-1 can lead to a variety of pituitary disorders, such as dwarfism due to GH deficiency, delayed puberty, and hypothyroidism due to TSH deficiency. Additionally, some studies have suggested that Pit-1 may also play a role in regulating energy balance and body weight, although the exact mechanisms are not fully understood.
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.
Hyperprolactinemia is a medical condition characterized by abnormally high levels of prolactin, a hormone produced by the pituitary gland. In women, this can lead to menstrual irregularities, milk production outside of pregnancy (galactorrhea), and infertility. In men, it can cause decreased libido, erectile dysfunction, breast enlargement (gynecomastia), and infertility. The condition can be caused by various factors, including pituitary tumors, certain medications, and hypothyroidism. Treatment typically involves addressing the underlying cause and may include medication to lower prolactin levels.
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.
"Molting" is not a term typically used in medical contexts. It is primarily used to describe the shedding and replacement of feathers, hair, or skin in animals, including birds, reptiles, insects, and other invertebrates. In humans and other mammals, this process is more commonly referred to as "shedding" or "growing new hair/skin."
However, if you are referring to the medical term "molt," it is a rare genetic disorder that affects the skin's pigmentation and causes it to shed in patches. It is also known as "congenital ichthyosiform erythroderma" or "non-bullous congenital ichthyosiform erythroderma." The condition is present at birth, and affected individuals have red, scaly skin that sheds in a pattern similar to snake skin. Molting is not contagious and has no known cure, but various treatments can help manage its symptoms.
Acromegaly is a rare hormonal disorder that typically occurs in middle-aged adults. It results from the pituitary gland producing too much growth hormone (GH) during adulthood. The excessive production of GH leads to abnormal growth of body tissues, particularly in the hands, feet, and face.
The term "acromegaly" is derived from two Greek words: "akros," meaning extremities, and "megaly," meaning enlargement. In most cases, acromegaly is caused by a benign tumor (adenoma) of the pituitary gland, which results in overproduction of GH.
Common symptoms include enlarged hands and feet, coarse facial features, deepened voice, joint pain, and sweating. If left untreated, acromegaly can lead to serious complications such as diabetes, hypertension, heart disease, and arthritis. Treatment usually involves surgical removal of the tumor, radiation therapy, or medication to control GH production.
Pituitary hormone-regulating hormone receptors refer to specific protein structures found on the surface of certain cells in the body. These receptors are responsible for detecting and responding to hormones produced by the hypothalamus, which regulate the function of the pituitary gland.
The pituitary gland is a small gland located at the base of the brain that plays a critical role in regulating various bodily functions, including growth and development, metabolism, reproduction, and stress response. The hypothalamus produces hormones that either stimulate or inhibit the release of pituitary hormones, which then act on target organs throughout the body to regulate their function.
Pituitary hormone-regulating hormone receptors are found on the surface of pituitary cells and are specific to individual hypothalamic hormones. When a hypothalamic hormone binds to its corresponding receptor, it triggers a series of intracellular signals that ultimately result in the release or inhibition of pituitary hormones.
Examples of pituitary hormone-regulating hormone receptors include:
* Thyroid-stimulating hormone (TSH) receptor, which responds to thyrotropin-releasing hormone (TRH) from the hypothalamus.
* Adrenocorticotropic hormone (ACTH) receptor, which responds to corticotropin-releasing hormone (CRH) from the hypothalamus.
* Growth hormone-releasing hormone (GHRH) receptor, which responds to GHRH from the hypothalamus.
* Gonadotropin-releasing hormone (GnRH) receptor, which responds to GnRH from the hypothalamus.
* Prolactin-inhibiting hormone (PIH) receptor, which responds to dopamine from the hypothalamus.
Abnormalities in pituitary hormone-regulating hormone receptors can lead to various endocrine disorders, such as hypothyroidism, Cushing's disease, acromegaly, and infertility.
Pituitary neoplasms refer to abnormal growths or tumors in the pituitary gland, a small endocrine gland located at the base of the brain. These neoplasms can be benign (non-cancerous) or malignant (cancerous), with most being benign. They can vary in size and may cause various symptoms depending on their location, size, and hormonal activity.
Pituitary neoplasms can produce and secrete excess hormones, leading to a variety of endocrine disorders such as Cushing's disease (caused by excessive ACTH production), acromegaly (caused by excessive GH production), or prolactinoma (caused by excessive PRL production). They can also cause local compression symptoms due to their size, leading to headaches, vision problems, and cranial nerve palsies.
The exact causes of pituitary neoplasms are not fully understood, but genetic factors, radiation exposure, and certain inherited conditions may increase the risk of developing these tumors. Treatment options for pituitary neoplasms include surgical removal, radiation therapy, and medical management with drugs that can help control hormonal imbalances.
Nifedipine is an antihypertensive and calcium channel blocker medication. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve the supply of oxygen and nutrients to the heart. Nifedipine is used to treat high blood pressure (hypertension), angina (chest pain), and certain types of heart rhythm disorders.
In medical terms, nifedipine can be defined as: "A dihydropyridine calcium channel blocker that is used in the treatment of hypertension, angina pectoris, and Raynaud's phenomenon. It works by inhibiting the influx of calcium ions into vascular smooth muscle and cardiac muscle, which results in relaxation of the vascular smooth muscle and decreased workload on the heart."
Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.
"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.
Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.
It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.
Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.
Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.
Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.
These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.
Immunoenzyme techniques are a group of laboratory methods used in immunology and clinical chemistry that combine the specificity of antibody-antigen reactions with the sensitivity and amplification capabilities of enzyme reactions. These techniques are primarily used for the detection, quantitation, or identification of various analytes (such as proteins, hormones, drugs, viruses, or bacteria) in biological samples.
In immunoenzyme techniques, an enzyme is linked to an antibody or antigen, creating a conjugate. This conjugate then interacts with the target analyte in the sample, forming an immune complex. The presence and amount of this immune complex can be visualized or measured by detecting the enzymatic activity associated with it.
There are several types of immunoenzyme techniques, including:
1. Enzyme-linked Immunosorbent Assay (ELISA): A widely used method for detecting and quantifying various analytes in a sample. In ELISA, an enzyme is attached to either the capture antibody or the detection antibody. After the immune complex formation, a substrate is added that reacts with the enzyme, producing a colored product that can be measured spectrophotometrically.
2. Immunoblotting (Western blot): A method used for detecting specific proteins in a complex mixture, such as a protein extract from cells or tissues. In this technique, proteins are separated by gel electrophoresis and transferred to a membrane, where they are probed with an enzyme-conjugated antibody directed against the target protein.
3. Immunohistochemistry (IHC): A method used for detecting specific antigens in tissue sections or cells. In IHC, an enzyme-conjugated primary or secondary antibody is applied to the sample, and the presence of the antigen is visualized using a chromogenic substrate that produces a colored product at the site of the antigen-antibody interaction.
4. Immunofluorescence (IF): A method used for detecting specific antigens in cells or tissues by employing fluorophore-conjugated antibodies. The presence of the antigen is visualized using a fluorescence microscope.
5. Enzyme-linked immunosorbent assay (ELISA): A method used for detecting and quantifying specific antigens or antibodies in liquid samples, such as serum or culture supernatants. In ELISA, an enzyme-conjugated detection antibody is added after the immune complex formation, and a substrate is added that reacts with the enzyme to produce a colored product that can be measured spectrophotometrically.
These techniques are widely used in research and diagnostic laboratories for various applications, including protein characterization, disease diagnosis, and monitoring treatment responses.
Patch-clamp techniques are a group of electrophysiological methods used to study ion channels and other electrical properties of cells. These techniques were developed by Erwin Neher and Bert Sakmann, who were awarded the Nobel Prize in Physiology or Medicine in 1991 for their work. The basic principle of patch-clamp techniques involves creating a high resistance seal between a glass micropipette and the cell membrane, allowing for the measurement of current flowing through individual ion channels or groups of channels.
There are several different configurations of patch-clamp techniques, including:
1. Cell-attached configuration: In this configuration, the micropipette is attached to the outer surface of the cell membrane, and the current flowing across a single ion channel can be measured. This configuration allows for the study of the properties of individual channels in their native environment.
2. Whole-cell configuration: Here, the micropipette breaks through the cell membrane, creating a low resistance electrical connection between the pipette and the inside of the cell. This configuration allows for the measurement of the total current flowing across all ion channels in the cell membrane.
3. Inside-out configuration: In this configuration, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the inner surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in isolation from other cellular components.
4. Outside-out configuration: Here, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the outer surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in their native environment, but with the ability to control the composition of the extracellular solution.
Patch-clamp techniques have been instrumental in advancing our understanding of ion channel function and have contributed to numerous breakthroughs in neuroscience, pharmacology, and physiology.
Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:
Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.
Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.
Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.
"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.
Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.
Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.
Cyclic adenosine monophosphate (cAMP) is a key secondary messenger in many biological processes, including the regulation of metabolism, gene expression, and cellular excitability. It is synthesized from adenosine triphosphate (ATP) by the enzyme adenylyl cyclase and is degraded by the enzyme phosphodiesterase.
In the body, cAMP plays a crucial role in mediating the effects of hormones and neurotransmitters on target cells. For example, when a hormone binds to its receptor on the surface of a cell, it can activate a G protein, which in turn activates adenylyl cyclase to produce cAMP. The increased levels of cAMP then activate various effector proteins, such as protein kinases, which go on to regulate various cellular processes.
Overall, the regulation of cAMP levels is critical for maintaining proper cellular function and homeostasis, and abnormalities in cAMP signaling have been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.
Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is a laboratory technique used in molecular biology to amplify and detect specific DNA sequences. This technique is particularly useful for the detection and quantification of RNA viruses, as well as for the analysis of gene expression.
The process involves two main steps: reverse transcription and polymerase chain reaction (PCR). In the first step, reverse transcriptase enzyme is used to convert RNA into complementary DNA (cDNA) by reading the template provided by the RNA molecule. This cDNA then serves as a template for the PCR amplification step.
In the second step, the PCR reaction uses two primers that flank the target DNA sequence and a thermostable polymerase enzyme to repeatedly copy the targeted cDNA sequence. The reaction mixture is heated and cooled in cycles, allowing the primers to anneal to the template, and the polymerase to extend the new strand. This results in exponential amplification of the target DNA sequence, making it possible to detect even small amounts of RNA or cDNA.
RT-PCR is a sensitive and specific technique that has many applications in medical research and diagnostics, including the detection of viruses such as HIV, hepatitis C virus, and SARS-CoV-2 (the virus that causes COVID-19). It can also be used to study gene expression, identify genetic mutations, and diagnose genetic disorders.
Human Growth Hormone (HGH), also known as somatotropin, is a peptide hormone produced in the pituitary gland. It plays a crucial role in human development and growth by stimulating the production of another hormone called insulin-like growth factor 1 (IGF-1). IGF-1 promotes the growth and reproduction of cells throughout the body, particularly in bones and other tissues. HGH also helps regulate body composition, body fluids, muscle and bone growth, sugar and fat metabolism, and possibly heart function. It is essential for human development and continues to have important effects throughout life. The secretion of HGH decreases with age, which is thought to contribute to the aging process.
Research, in the context of medicine, is a systematic and rigorous process of collecting, analyzing, and interpreting information in order to increase our understanding, develop new knowledge, or evaluate current practices and interventions. It can involve various methodologies such as observational studies, experiments, surveys, or literature reviews. The goal of medical research is to advance health care by identifying new treatments, improving diagnostic techniques, and developing prevention strategies. Medical research is typically conducted by teams of researchers including clinicians, scientists, and other healthcare professionals. It is subject to ethical guidelines and regulations to ensure that it is conducted responsibly and with the best interests of patients in mind.
Somatotropin receptors are a type of cell surface receptor that binds to and gets activated by the hormone somatotropin, also known as growth hormone (GH). These receptors are found in many tissues throughout the body, including the liver, muscle, and fat. When somatotropin binds to its receptor, it activates a series of intracellular signaling pathways that regulate various physiological processes such as growth, metabolism, and cell reproduction.
Somatotropin receptors belong to the class I cytokine receptor family and are composed of two subunits, a homodimer of extracellular glycoproteins that bind to the hormone and an intracellular tyrosine kinase domain that activates downstream signaling pathways. Mutations in the somatotropin receptor gene can lead to growth disorders such as dwarfism or gigantism, depending on whether the mutation results in a decrease or increase in receptor activity.
Hormones are defined as chemical messengers that are produced by endocrine glands or specialized cells and are transported through the bloodstream to tissues and organs, where they elicit specific responses. They play crucial roles in regulating various physiological processes such as growth, development, metabolism, reproduction, and mood. Examples of hormones include insulin, estrogen, testosterone, adrenaline, and thyroxine.
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Adenomas5
- For the purpose of this review, only the more common lactotroph and somatotroph adenomas will be addressed. (cap.org)
- Somatotroph (GH) adenomas are nearly equally divided into densely and sparsely granulated types. (cap.org)
- The evaluation of ghrelin mRNA expression in human somatotroph adenomas. (nel.edu)
- We decided to determine the expression of ghrelin in somatotroph adenomas. (nel.edu)
- We therefore hypothesized that the physiological IGF-I-GH negative feedback loop may be reset in somatotroph adenomas, and we investigated the role of type 1 IGF receptor (IGF-R) and GH receptor (GHR) by quantifying mRNA expression in somatotroph tumours, and investigated the possible presence of mutations of the GHR gene.Methods: Pituitary t. (endocrine-abstracts.org)
Pituitary Gland3
- Growth hormone is a complex chain of about 190 amino acids that are secreted by special cells called the somatotrophs in the pituitary gland. (myelin.org)
- The CJC-1295 and GHRP-6 blend combines two peptides that may interact with calls in the pituitary gland and the hypothalamus called somatotrophs. (biotechpeptides.com)
- Amplifying GHRH signaling in somatotrophs of the anterior pituitary gland. (aelart.com)
Anterior4
- 1 More than 95% of cases are caused by autonomous secretion of GH from anterior pituitary tumours and result in clonal expansion of somatotrophs. (hkmj.org)
- Somatotrophs, anterior pituitary cells, synthesize and secrete HGH. (gilmorehealth.com)
- Somatotrophs are cells in the anterior pituitary that release pituitary growth hormone. (ultimapharmaceuticals.com)
- These are synthesized and produced by cells (somatotrophs) inside the anterior pituitary. (healthcareguys.com)
MRNA expression1
- Human pituitary somatotroph adenoma tissues were obtained at the time of transsphenoidal surgery from 3 acromegalic patients and studied for ghrelin mRNA expression. (nel.edu)
Cells7
- Combining these peptides may enhance both the amplitude and the frequency of the growth hormone pulses by somatotroph cells. (biotechpeptides.com)
- CJC-1295 appears to target somatotroph cells by potentially interacting with the GHRH receptor they express. (biotechpeptides.com)
- Phosphorylated transcription factors may enter the nucleus of somatotroph cells, potentially influencing genes related to growth hormone synthesis. (biotechpeptides.com)
- [7] Ultimately, CJC-1295 binding appears to trigger events leading to the release of growth hormone from vesicles by the somatotroph cells. (biotechpeptides.com)
- By electron microscopy five types of secretory cells (somatotrophs, mammotrophs, thyrotrophs, gonadotrophs, and corticotrophs) plus endothelial and follicular cells can be identified and are morphologically well preserved up to 20 h after dissociation. (rupress.org)
- Growth Hormone Releasing Hormone (GHRH)- Released by the brain to tell your body's growth hormone storage cells (somatotrophs) to release growth hormone. (brigittaplosz.net)
- and tells your cells (somatotrophs) to cease growth hormone release. (brigittaplosz.net)
GHRH1
- Ghrelin (GHR) may also influence GH secretion by acting directly on somatotrophs or through stimulatory effects on GHRH neurons. (endotext.org)
Growth4
- Acromegaly is a rare, chronic disease caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma. (bmj.com)
- It is caused by excessive secretion of growth hormone, usually due to a pituitary somatotroph adenoma. (bmj.com)
- Somatotrophs - growth hormone (GH). (histologyguide.com)
- Growth Hormone Releasing Peptide-6 (GHRP-6) is a synthetic hexapeptide, which specifically stimulates secretion of growth hormone by pituitary somatotrophs. (ultimapharmaceuticals.com)
Secretion1
- Sulphonylureas stimulate GH secretion and this study was undertaken to investigate the possible stimulatory effect of repaglinide and nateglinide, two novel oral glucose regulators, on critical steps of the stimulus-secretion coupling in single rat somatotrophs. (ox.ac.uk)
Descriptor1
- Somatotrophs" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
Release1
- GH release was measured from perifused rat somatotrophs. (ox.ac.uk)
Action1
- Both compounds induced action potential firing in the somatotrophs irrespective of whether GH-releasing hormone was present or not. (ox.ac.uk)
Lactotrophs6
- At the pituitary level, follistatin signals could be located in carp somatotrophs, gonadotrophs, and lactotrophs. (frontiersin.org)
- The model behavior resembles that seen in somatotrophs, lactotrophs, and corticotrophs. (nih.gov)
- thyroid-stimulating hormone (TSH) producing thyrotrophs, growth hormone (GH) producing somatotrophs, prolactin (PRL) producing lactotrophs, and follicle-stimulating hormone (FSH) and luteinizing hormone (LH) producing gonadotrophs. (nih.gov)
- The secretory functions of somatotrophs and lactotrophs are also negatively controlled by hypothalamic somatostatin and dopamine, respectively. (nih.gov)
- Lactotrophs, somatotrophs, thyrotrophs, corticotrophs and gonadotrophs in the anterior pituitary gland secrete the polypeptide hormones prolactin (PRL), growth hormone (GH), thyroid stimulating hormone (TSH), adrenocorticotropic hormone (ACTH) and luteinizing (LH). (endocrine-abstracts.org)
- Somatotrophs and lactotrophs are acidophils that secrete GH and PRL, respectively, whereas mammosomatotrophs secrete both GH and PRL. (oncohemakey.com)
Adenoma2
- 3. Somatotroph hyperplasia without pituitary adenoma associated with a long standing growth hormone-releasing hormone-producing bronchial carcinoid. (nih.gov)
- 5. Pituitary somatotroph adenoma producing growth hormone (GH)-releasing hormone (GHRH) with an elevated plasma GHRH concentration: a model case for autocrine and paracrine regulation of GH secretion by GHRH. (nih.gov)
Hyperplasia and acromegaly2
- Primary pituitary diffuse large B-cell lymphoma with somatotroph hyperplasia and acromegaly: case report. (harvard.edu)
- 1. A growth hormone-releasing hormone-producing pancreatic islet cell tumor metastasized to the pituitary is associated with pituitary somatotroph hyperplasia and acromegaly. (nih.gov)
Gonadotrophs1
- 12. Growth hormone-releasing hormone and glucocorticoids determine the balance between luteinising hormone (LH) beta- and LH beta/follicle-stimulating hormone beta-positive gonadotrophs and somatotrophs in the 14-day-old rat pituitary tissue in aggregate cell culture. (nih.gov)
Growth4
- 2. Acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma. (nih.gov)
- Released from the somatotroph cells within the lateral wings of the brain's anterior pituitary gland, GH, a protein-based, 191-amino acid polypeptide, controls many bodily processes - from fat loss to bone growth to muscle building. (allmaxnutrition.com)
- INTRODUCTIONGrowth Hormone (GH) and Growth Hormone Deficiency (GHD): GH is secreted from adenohypophysis present on the somatotrophs. (gerardcambon.net)
- ABSTRACT: In rat pituitary somatotrophs, cytochrome oxidase is co-packaged with growth hormone (GH) in some storage granules. (pharmalight.eu)
Acromegaly1
- Clinical, hormonal and pathomorphological markers of somatotroph pituitary neuroendocrine tumors predicting the treatment outcome in acromegaly. (nih.gov)
Amino acids1
- It is being made from 191 amino acids, also known as somatotrophs. (supplementpolice.com)
ACTH1
- ACTH co-secretion by a mammo-somatotroph pituitary tumor can be clinically significant but phenotypically unidentifiable. (nih.gov)
Function1
- Cellular function of somatotroph cell. (endotext.org)
Treatment1
- Pathological markers of somatotroph pituitary neuroendocrine tumors predicting the response to medical treatment. (nih.gov)