NCI's Dictionary of Cancer Terms provides easy-to-understand definitions for words and phrases related to cancer and medicine.
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Gonadotrophin-releasing hormone is released from nerve cells in the brain. It controls the production of luteinising hormone and follicle stimulating hormone from the pituitary gland.
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Gonadotropin-releasing hormone (GnRH) is critical to sexual development and a healthy reproductive system. It helps your body make testosterone and estrogen.
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Gonadotropin-releasing hormone (GnRH) is critical to sexual development and a healthy reproductive system. It helps your body make testosterone and estrogen.
View more »
Gonadotropin-releasing hormone (GnRH) is critical to sexual development and a healthy reproductive system. It helps your body make testosterone and estrogen.
View more »
Gonadotropin-releasing hormone (GnRH) is critical to sexual development and a healthy reproductive system. It helps your body make testosterone and estrogen.
View more »
Gonadotropin-releasing hormone (GnRH) is critical to sexual development and a healthy reproductive system. It helps your body make testosterone and estrogen.
View more »
Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) orchestrate the reproduction cycle and regulate the sex steroid secretion from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neurotransmitters/peptides in a variety of tissues, where the peptides exert many different effects. mRNA coding for GnRH1 and GnRH2 have been described in the human gastrointestinal tract, and GnRH has been found in both submucosal and myenteric neurons. mRNA coding for GnRH and the fully expressed peptide have been found in rat enteric neurons by some researchers but not by others. mRNA coding for GnRH receptors, but not the fully expressed receptor, has been found in one rat study. GnRH influences gastrointestinal motility and secretion. GnRH analogs are clinically used in the treatment of sex hormone-dependent diseases, i.e., endometriosis and malignancies, and as pretreatment for in vitro fertilization (IVF). Reduced numbers of enteric neurons and IgM antibodies against GnRH and progonadoliberin-2 (precursor of GnRH2) have been observed after such treatment, with the clinical picture of gastrointestinal dysmotility. Similarly, a rat model of enteric neurodegeneration has been developed after administration of the GnRH analog buserelin. Serum IgM antibodies against GnRH1, progonadoliberin-2, and GnRH receptors have been described in patients with signs and symptoms of gastrointestinal dysmotility and/or autonomic dysfunction, such as irritable bowel syndrome (IBS), enteric dysmotility, diabetes mellitus, and primary Sjögren´s syndrome. Thus, apart from regulation of reproduction and sex hormone secretion, GnRH also constitute a part of ENS and its functions during physiological and pathological conditions. This review aimed to describe the role of GnRH in the enteric nervous system (ENS).
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Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) orchestrate the reproduction cycle and regulate the sex steroid secretion from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neurotransmitters/peptides in a variety of tissues, where the peptides exert many different effects. mRNA coding for GnRH1 and GnRH2 have been described in the human gastrointestinal tract, and GnRH has been found in both submucosal and myenteric neurons. mRNA coding for GnRH and the fully expressed peptide have been found in rat enteric neurons by some researchers but not by others. mRNA coding for GnRH receptors, but not the fully expressed receptor, has been found in one rat study. GnRH influences gastrointestinal motility and secretion. GnRH analogs are clinically used in the treatment of sex hormone-dependent diseases, i.e., endometriosis and malignancies, and as pretreatment for in vitro fertilization (IVF). Reduced numbers of enteric neurons and IgM antibodies against GnRH and progonadoliberin-2 (precursor of GnRH2) have been observed after such treatment, with the clinical picture of gastrointestinal dysmotility. Similarly, a rat model of enteric neurodegeneration has been developed after administration of the GnRH analog buserelin. Serum IgM antibodies against GnRH1, progonadoliberin-2, and GnRH receptors have been described in patients with signs and symptoms of gastrointestinal dysmotility and/or autonomic dysfunction, such as irritable bowel syndrome (IBS), enteric dysmotility, diabetes mellitus, and primary Sjögren´s syndrome. Thus, apart from regulation of reproduction and sex hormone secretion, GnRH also constitute a part of ENS and its functions during physiological and pathological conditions. This review aimed to describe the role of GnRH in the enteric nervous system (ENS).
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Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) orchestrate the reproduction cycle and regulate the sex steroid secretion from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neurotransmitters/peptides in a variety of tissues, where the peptides exert many different effects. mRNA coding for GnRH1 and GnRH2 have been described in the human gastrointestinal tract, and GnRH has been found in both submucosal and myenteric neurons. mRNA coding for GnRH and the fully expressed peptide have been found in rat enteric neurons by some researchers but not by others. mRNA coding for GnRH receptors, but not the fully expressed receptor, has been found in one rat study. GnRH influences gastrointestinal motility and secretion. GnRH analogs are clinically used in the treatment of sex hormone-dependent diseases, i.e., endometriosis and malignancies, and as pretreatment for in vitro fertilization (IVF). Reduced numbers of enteric neurons and IgM antibodies against GnRH and progonadoliberin-2 (precursor of GnRH2) have been observed after such treatment, with the clinical picture of gastrointestinal dysmotility. Similarly, a rat model of enteric neurodegeneration has been developed after administration of the GnRH analog buserelin. Serum IgM antibodies against GnRH1, progonadoliberin-2, and GnRH receptors have been described in patients with signs and symptoms of gastrointestinal dysmotility and/or autonomic dysfunction, such as irritable bowel syndrome (IBS), enteric dysmotility, diabetes mellitus, and primary Sjögren´s syndrome. Thus, apart from regulation of reproduction and sex hormone secretion, GnRH also constitute a part of ENS and its functions during physiological and pathological conditions. This review aimed to describe the role of GnRH in the enteric nervous system (ENS).
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Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) orchestrate the reproduction cycle and regulate the sex steroid secretion from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neurotransmitters/peptides in a variety of tissues, where the peptides exert many different effects. mRNA coding for GnRH1 and GnRH2 have been described in the human gastrointestinal tract, and GnRH has been found in both submucosal and myenteric neurons. mRNA coding for GnRH and the fully expressed peptide have been found in rat enteric neurons by some researchers but not by others. mRNA coding for GnRH receptors, but not the fully expressed receptor, has been found in one rat study. GnRH influences gastrointestinal motility and secretion. GnRH analogs are clinically used in the treatment of sex hormone-dependent diseases, i.e., endometriosis and malignancies, and as pretreatment for in vitro fertilization (IVF). Reduced numbers of enteric neurons and IgM antibodies against GnRH and progonadoliberin-2 (precursor of GnRH2) have been observed after such treatment, with the clinical picture of gastrointestinal dysmotility. Similarly, a rat model of enteric neurodegeneration has been developed after administration of the GnRH analog buserelin. Serum IgM antibodies against GnRH1, progonadoliberin-2, and GnRH receptors have been described in patients with signs and symptoms of gastrointestinal dysmotility and/or autonomic dysfunction, such as irritable bowel syndrome (IBS), enteric dysmotility, diabetes mellitus, and primary Sjögren´s syndrome. Thus, apart from regulation of reproduction and sex hormone secretion, GnRH also constitute a part of ENS and its functions during physiological and pathological conditions. This review aimed to describe the role of GnRH in the enteric nervous system (ENS).
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Gonadotropin-releasing hormone (GnRH), a decapeptide, is a part of the hypothalamic-pituitary-gonadal axis, and being a part of this system makes it vital for human reproduction. Since its discovery by a group of Nobel laureate Andrew V. Schally in 1971 from porcine hypothalamus as one of the earliest hypothalamic releasing hormones, it has been a center of attention of research scientists because of its central role in reproduction not only in humans but also in all vertebrates.
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Gonadotropin hormone-releasing hormone (GnRH) is the key regulator of the reproductive axis. Its pulsatile secretion determines the pattern of secretion of the gonadotropins follicle stimulating hormone and luteinizing hormone, which then regulate both the endocrine function and gamete maturation in the gonads. Recent years have seen rapid developments in how GnRH secretion is regulated, with the discovery of the kisspeptin-neurokinin-dynorphin neuronal network in the hypothalamus. This mediates both positive and negative sex steroid feedback control of GnRH secretion, in conjunction with other neuropeptides and neurotransmitters. This review describes the main features of this regulatory system, including how its anatomical arrangements interact with functional control, and describes key differences between rodent and larger mammalian systems. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.
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GnRH I | C60H73N15O13 | CID 16132914 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
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gonadotropin-releasing hormone (GnRH), also known as luteinizing hormone-releasing hormone, a neurohormone consisting of 10 amino acids that is produced in the arcuate nuclei of the hypothalamus. GnRH stimulates the synthesis and secretion of the two gonadotropins—luteinizing hormone (LH) and follicle-stimulating hormone (FSH)—by the anterior pituitary gland. The effects of GnRH on the secretion of LH and FSH are not exactly parallel, and the variations are probably due to other modulating factors such as the serum concentrations of steroid hormones (substances secreted by the adrenal cortex, testes, and ovaries). Characteristic of all releasing hormones and most striking in the case of
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Gonadotropin-releasing hormone (GnRH) stimulates the synthesis and release of gonadotropins, which induce estrogen production and subsequent ovulation. Therefore, long-term GnRH exposure to regulate ovarian hyperstimulation is recognized as the gold standard for most in vitro fertilization (IVF) strategies. However, one of the most disappointing aspects of current IVF technology is relatively low rate (between 35 and 50%) of positive pregnancy outcomes, and the major reason for this high cancellation rate has not yet been revealed. Previous studies have demonstrated that resident stem cell deficiency limits the cyclic regenerative capacity of the endometrium and subsequently increases pregnancy failure rates. Therefore, we hypothesized that long-term GnRH exposure directly damages endometrial stem cells and consequently negatively affects pregnancy outcomes in GnRH-based IVF. In addition to their well-known roles in regulating the hypothalamus-pituitary-gonadal axis, GnRH and its receptors also localize in the extra-hypothalamic endometrium, suggesting a possible non-canonical role in endometrial stem cells. Consistent with our hypothesis, we show for the first time that GnRH suppresses the multiple beneficial functions of endometrial stem cells via the PI3K/Akt signaling pathway in vitro and in vivo. To the best of our knowledge, this is the first study to focus on the direct effects of GnRH on the regenerative potential of stem cells, and the findings will facilitate the development of more promising IVF strategies.
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Gonadotropin-releasing hormone (GnRH) stimulates the synthesis and release of gonadotropins, which induce estrogen production and subsequent ovulation. Therefore, long-term GnRH exposure to regulate ovarian hyperstimulation is recognized as the gold standard for most in vitro fertilization (IVF) strategies. However, one of the most disappointing aspects of current IVF technology is relatively low rate (between 35 and 50%) of positive pregnancy outcomes, and the major reason for this high cancellation rate has not yet been revealed. Previous studies have demonstrated that resident stem cell deficiency limits the cyclic regenerative capacity of the endometrium and subsequently increases pregnancy failure rates. Therefore, we hypothesized that long-term GnRH exposure directly damages endometrial stem cells and consequently negatively affects pregnancy outcomes in GnRH-based IVF. In addition to their well-known roles in regulating the hypothalamus-pituitary-gonadal axis, GnRH and its receptors also localize in the extra-hypothalamic endometrium, suggesting a possible non-canonical role in endometrial stem cells. Consistent with our hypothesis, we show for the first time that GnRH suppresses the multiple beneficial functions of endometrial stem cells via the PI3K/Akt signaling pathway in vitro and in vivo. To the best of our knowledge, this is the first study to focus on the direct effects of GnRH on the regenerative potential of stem cells, and the findings will facilitate the development of more promising IVF strategies.
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Gonadotropin-releasing hormone (GnRH) stimulates the synthesis and release of gonadotropins, which induce estrogen production and subsequent ovulation. Therefore, long-term GnRH exposure to regulate ovarian hyperstimulation is recognized as the gold standard for most in vitro fertilization (IVF) strategies. However, one of the most disappointing aspects of current IVF technology is relatively low rate (between 35 and 50%) of positive pregnancy outcomes, and the major reason for this high cancellation rate has not yet been revealed. Previous studies have demonstrated that resident stem cell deficiency limits the cyclic regenerative capacity of the endometrium and subsequently increases pregnancy failure rates. Therefore, we hypothesized that long-term GnRH exposure directly damages endometrial stem cells and consequently negatively affects pregnancy outcomes in GnRH-based IVF. In addition to their well-known roles in regulating the hypothalamus-pituitary-gonadal axis, GnRH and its receptors also localize in the extra-hypothalamic endometrium, suggesting a possible non-canonical role in endometrial stem cells. Consistent with our hypothesis, we show for the first time that GnRH suppresses the multiple beneficial functions of endometrial stem cells via the PI3K/Akt signaling pathway in vitro and in vivo. To the best of our knowledge, this is the first study to focus on the direct effects of GnRH on the regenerative potential of stem cells, and the findings will facilitate the development of more promising IVF strategies.
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Gonadotropin-releasing hormone (GnRH) stimulates the synthesis and release of gonadotropins, which induce estrogen production and subsequent ovulation. Therefore, long-term GnRH exposure to regulate ovarian hyperstimulation is recognized as the gold standard for most in vitro fertilization (IVF) strategies. However, one of the most disappointing aspects of current IVF technology is relatively low rate (between 35 and 50%) of positive pregnancy outcomes, and the major reason for this high cancellation rate has not yet been revealed. Previous studies have demonstrated that resident stem cell deficiency limits the cyclic regenerative capacity of the endometrium and subsequently increases pregnancy failure rates. Therefore, we hypothesized that long-term GnRH exposure directly damages endometrial stem cells and consequently negatively affects pregnancy outcomes in GnRH-based IVF. In addition to their well-known roles in regulating the hypothalamus-pituitary-gonadal axis, GnRH and its receptors also localize in the extra-hypothalamic endometrium, suggesting a possible non-canonical role in endometrial stem cells. Consistent with our hypothesis, we show for the first time that GnRH suppresses the multiple beneficial functions of endometrial stem cells via the PI3K/Akt signaling pathway in vitro and in vivo. To the best of our knowledge, this is the first study to focus on the direct effects of GnRH on the regenerative potential of stem cells, and the findings will facilitate the development of more promising IVF strategies.
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Gonadotropin-releasing hormone (GnRH) is a neurohormone central to initiation of the reproductive hormone cascade. Pulsatile secretion of GnRH from the hypothalamus is key in establishing and maintaining normal gonadal function.
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Compare gonadotropin releasing hormones. View important safety information, ratings, user reviews, popularity and more.
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Background: Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) are involved in the reproductive cycle and regulate the secretion of sex steroids from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neuropeptides in a variet
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a hormone secreted by the hypothalamus that stimulates the anterior lobe of the pituitary gland to release gonadotropins (such as luteinizing hormone and follicle-stimulating hormone) —abbreviation GnRH—called also luteinizing hormone-releasing hormone… See the full definition
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GnRH is the hypothalamic main regulator of the hypothalamic-pituitary-gonadal reproductive axis, but it was found to exert additional functions due to the wide distribution of its receptors both in central nervous system (from cortex to spinal cord) and in peripheral organs and tissues. The possible activity of GnRH/GnRHR system at the level of the hippocampus has raised the interest on the effects of the decapeptide and its analogues on neurogenesis and neuronal functions. Recently, has been observed that GnRH is decreased in mice hypothalamic ageing and that restoring normal GnRH levels may attenuate brain and systemic aging processes. Other studies have also pointed out on neurogenic and neuro protective actions of GnRH in several models of neurodegeneration, as in Alzheimer’s disease and in spinal cord injury models. A direct effect of GnRH on cholesterol and estrogen synthesis in human neuronal-like cells has been also proposed as a mechanism involved in neuro protective activity. Since GnRH analogues are known to be safe and effective, a new possible lines of therapeutic intervention to control some of the defects present in aging and neurodegenerative diseases may be delineated. In conclusion, brain GnRH/GnRHR system is a novel and extremely interesting target, since it mediates many pleiotropic actions possibly integrated in a complex control of reproductive functions with neurogenesis, neuroprotection, sex behavior and cognition.GnRH is the hypothalamic main regulator of the hypothalamic-pituitary-gonadal reproductive axis, but it was found to exert additional functions due to the wide distribution of its receptors both in central nervous system (from cortex to spinal cord) and in peripheral organs and tissues. The possible activity of GnRH/GnRHR system at the level of the hippocampus has raised the interest on the effects of the decapeptide and its analogues on neurogenesis and neuronal functions. Recently, has been observed that GnRH is decreased in mice hypothalamic ageing and that restoring normal GnRH levels may attenuate brain and systemic aging processes. Other studies have also pointed out on neurogenic and neuro protective actions of GnRH in several models of neurodegeneration, as in Alzheimer’s disease and in spinal cord injury models. A direct effect of GnRH on cholesterol and estrogen synthesis in human neuronal-like cells has been also proposed as a mechanism involved in neuro protective activity. Since GnRH analogues are known to be safe and effective, a new possible lines of therapeutic intervention to control some of the defects present in aging and neurodegenerative diseases may be delineated. In conclusion, brain GnRH/GnRHR system is a novel and extremely interesting target, since it mediates many pleiotropic actions possibly integrated in a complex control of reproductive functions with neurogenesis, neuroprotection, sex behavior and cognition.
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Gonadotropin-releasing hormone (GnRH) helps trigger puberty & keeps men & women fertile as adults. Learn more about GnRH function & more.
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