Journal articles on the topic 'Gonadotrophins'
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1
Tasaka, K., N. Masumoto, J. Mizuki, Y. Ikebuchi, M. Ohmichi, H. Kurachi, A. Miyake, and Y. Murata. "Rab3B is essential for GnRH-induced gonadotrophin release from anterior pituitary cells." Journal of Endocrinology 157, no. 2 (May 1, 1998): 267–74. http://dx.doi.org/10.1677/joe.0.1570267.
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Gonadotrophin-releasing hormone (GnRH) induces the release of gonadotrophins via an increase in cytosolic Ca2+ concentration ([Ca2+]). Rab3B, a member of the small GTP-binding protein Rab family, is known to be involved in Ca(2+)-regulated exocytosis in pituitary cells. However, it is not known whether Rab3B functions in the physiological process regulated by GnRH in gonadotrophs. In this study using antisense oligonucleotide against Rab3B (AS-Rab3B) we determined that Rab3B is involved in GnRH-induced gonadotrophin release. Rab3B immunopositive cells were reduced in 24% of pituitary cells by AS-Rab3B. This treatment did not affect the population of gonadotrophs or the intracellular contents of gonadotrophins. However, AS-Rab3B significantly inhibited the total amount of basal and GnRH-induced gonadotrophin released from pituitary cells. These results show that Rab3B is involved in basal and GnRH-induced gonadotrophins release but not the storage of gonadotrophins. Next, the changes in [Ca2+] and exocytosis in gonadotrophs treated with AS-Rab3B were compared among Rab3B-positive and -negative cells. The change in [Ca2+] was not different in the two groups, but exocytosis was significantly inhibited in Rab3B-negative cells. These results suggest that Rab3B is essential for GnRH-regulated exocytosis downstream of cytosolic Ca2+ in gonadotrophs.
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Huhtaniemi, Ilpo, and Maria Alevizaki. "Gonadotrophic Hormones – An Overview of their Involvement in Gonadal and Extragonadal Tumours." European Endocrinology 7, no. 1 (2010): 8. http://dx.doi.org/10.17925/ee.2011.07.01.8.
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The concept of the direct involvement of gonadotrophins in tumorigenesis has been around for a long time. First, because the gonads are direct targets of gonadotrophin action, their tumours have been proposed to be gonadotrophin-dependent. Second, the recent findings of gonadotrophin receptors in extragonadal tissues has prompted the hypothesis that some extragonadal tumours (e.g. breast, uterus, prostate, pituitary and adrenal) could also be under the direct regulatory action of gonadotrophins. However, although supported by numerousin vitroexperiments and experimental animal models, the clinical evidence for a direct tumorigenic role of gonadotrophins remains weak. The purpose of this brief review is to present a critical evaluation of current information, both clinical and experimental, about the involvement of gonadotrophins in the induction and growth of gonadal and extragonadal tumours.
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Meeran, Dawud, Henryk F. Urbanski, Susan J. Gregory, Julie Townsend, and Domingo J. Tortonese. "Developmental Changes in the Hormonal Identity of Gonadotroph Cells in the Rhesus Monkey Pituitary Gland." Journal of Clinical Endocrinology & Metabolism 88, no. 6 (June 1, 2003): 2934–42. http://dx.doi.org/10.1210/jc.2002-021001.
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To help elucidate the regulatory mechanism responsible for divergent gonadotrophin secretion during sexual maturation, we examined the gonadotroph population and hormonal identity of gonadotroph subtypes in pituitary glands of juvenile (age, 1.7 ± 0.2 yr) and adult (age, 12.3 ± 0.8 yr) male rhesus monkeys (Macacca mulatta). Serum LH and testosterone concentrations were, respectively, 3 and 7 times lower in juveniles than in adults, thus confirming the different stages of development. Immunohistochemistry revealed that the proportion of LH gonadotrophs in relation to the total pituitary cell population in the juvenile animals was significantly smaller than in the adults. In a subsequent study, double immunofluorescent labeling identified three distinct gonadotroph subtypes in both age groups: ones expressing either LH or FSH and another one expressing a combination of both gonadotrophins. Whereas the number of monohormonal LH cells per unit area was greater in the adults than in the juveniles, the number of monohormonal FSH gonadotrophs was remarkably lower. However, the proportion of FSH cells (whether mono- or bihormonal) within the gonadotroph population was similar between groups. Interestingly, the proportion and number of bihormonal gonadotrophs as well as the LH/FSH gonadotroph ratio were significantly greater in the adults than in the juveniles. Taken together, these data reveal that during the juvenile-adult transition period, not only does the pituitary gonadotroph population increase, but a large number of monohormonal FSH gonadotrophs are likely to become bihormonal. Because this morphological switch occurs when marked changes in plasma gonadotrophins are known to occur, it may represent an intrapituitary mechanism that differentially regulates gonadotrophin secretion during sexual development.
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Rulli, Susana B., and Ilpo Huhtaniemi. "What have gonadotrophin overexpressing transgenic mice taught us about gonadal function?" Reproduction 130, no. 3 (September 2005): 283–91. http://dx.doi.org/10.1530/rep.1.00661.
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The two gonadotrophins, follicle-stimulating hormone and luteinising hormone, are pivotal regulators of the development and maintenance of normal fertility by maintaining testicular and ovarian endocrine function and gametogenesis. Too low gonadotrophin secretion, i.e. hypogonadotrophic hypogonadism, is a common cause of infertility. But there are also physiological and pathophysiological conditions where gonadotrophin secretion and/or action are either transiently or chronically elevated, such as pregnancy, pituitary tumours, polycystic ovarian syndrome, activating gonadotrophin receptor mutations, perimenopause and menopause. These situations can be either the primary or secondary cause of infertility and gonadal pathologies in both sexes. Also the role of gonadotrophins as tumour promoters is possible. Recently, the possibility to combine information from genetically modified mice and human phenotypes in connection with mutations of gonadotrophin or gonadotrophin receptor genes has elucidated many less well known mechanisms involved in dysregulation of gonadotrophin function. Among the genetically modified mouse models, transgenic mice with gonadotrophin hypersecretion have been developed during the last few years. In this review, we describe the key findings on transgenic mouse models overexpressing gonadotrophins and present their possible implications in related human pathologies. In addition, we provide examples of genetic mouse models with secondary effects on gonadotrophin production and, consequently, on gonadal function.
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Kotsuji, F., K. Hosokawa, and T. Tominaga. "Effects of the daily administration of gonadotrophin-releasing hormone on the anterior pituitary gland of rats with restricted feeding." Journal of Endocrinology 134, no. 2 (August 1992): 177—NP. http://dx.doi.org/10.1677/joe.0.1340177.
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ABSTRACT To investigate the influence of weight reduction on pituitary function and its modulation by gonadotrophin-releasing hormone (GnRH), female rats were restricted to 10 g food/day for 60 days. GnRH (5 μg) or saline (0·2 ml) were administered daily between days 31 and 60 of the period of underfeeding. Underfeeding brought about a decrease in the pituitary gonadotrophin content, serum levels of gonadotrophins and oestradiol, and the number and size of both LH- and FSH-positive pituitary cells. The administration of GnRH to underfed rats produced an increase in the pituitary and serum gonadotrophin levels and the number and size of both LH- and FSH-positive pituitary cells. These observations suggest that underfeeding and/or weight loss diminish the number and activity of the pituitary gonadotrophs, and that daily administration of GnRH both increases the number of gonadotrophs and augments their activity. Journal of Endocrinology (1992) 134, 177–182
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Waterhouse, Tracey, Shae-Lee Cox, Melanie Snow, Graham Jenkin, and Jill Shaw. "Offspring produced from heterotopic ovarian allografts in male and female recipient mice." Reproduction 127, no. 6 (June 2004): 689–94. http://dx.doi.org/10.1530/rep.1.00081.
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Studies on human ovarian xenografts and mouse allografts indicate that the male hormonal milieu and exogenous gonadotrophin administration stimulate antral follicle growth. However, it is not known whether oocytes produced under these conditions are developmentally competent. The objective of our study was to evaluate the developmental competence of oocytes produced in heterotopic mouse ovarian grafts placed in male and female recipient mice. Gonadotrophins were 7.5 IU pregnant mare serum gonadotrophin (PMSG) alone or 7.5 IU PMSG and 7.5 IU human chorionic gonadotrophin or were not given prior to oocyte collection. The developmental competence of oocytes was assessed by performing in vitro fertilisation and embryo transfer to recipients. When no gonadotrophins were given the cleavage rate was similar for oocytes collected from ovarian grafts in male and female recipients. Gonadotrophin treatment significantly (P < 0.05) increased two-cell formation by oocytes grown in female graft recipients but not in male recipients. Implantation rates, fetal development and the birth of live young were unaffected by the sex of the graft recipient or gonadotrophin treatment. Live offspring were produced from oocytes collected from ovarian grafts in male and female recipients treated with or without gonadotrophins. In conclusion, this work has shown that the hormonal environment of male mice can support the growth of oocytes in ovarian allografts and that these oocytes can produce live offspring.
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Jamal Uddin, Md, and S. Bhattacharya. "In-vitro binding of gonadotrophin to fish ovary." Journal of Endocrinology 111, no. 3 (December 1986): 407–13. http://dx.doi.org/10.1677/joe.0.1110407.
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ABSTRACT Binding of piscine and mammalian gonadotrophin to plasma membranes from the ovaries of a fish, the murrel (Channa punctatus), clearly suggests that the fish ovary possesses distinct and specific binding sites for both piscine and mammalian gonadotrophins. Maximum specific binding of 125I-labelled human chorionic gonadotrophin (125I-hCG) and 125I-labelled silver carp gonadotrophin (125I-scG) was obtained at 30 °C and pH 7·5 during 2 h of incubation. In competitive binding studies, binding of radiolabelled scG was effectively inhibited by piscine gonadotrophins while LH and hCG had less effect and FSH showed no inhibition. By using plasma membrane preparations from kidney, skeletal muscle, brain and ovary it could be shown that specific binding of radiolabelled gonadotrophins was restricted to ovarian tissue. Binding characteristics of both 125I-scG and 125I-hCG to a preparation of murrel ovarian plasma membranes showed saturability with high affinity and low capacity. Scatchard plot analysis gave a higher dissociation constant for hCG (Kd = 235 pmol/l) than for scG (Kd= 127 pmol/l). Maximum binding capacity of scG was about twofold higher (6·27 fmol/mg protein) than that of hCG (3·76 fmol/mg protein). An increase in gonadotrophin binding resulted in a greater formation of pregnenolone from cholesterol, indicating functional relevance. At a concentration of 8 mmol/l, Ca2+ markedly inhibited the binding of gonadotrophin. The physiological importance of this inhibition is discussed. J. Endocr. (1986) 111, 407–413
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Miller, D. W., and A. N. Brooks. "Placental steroids are involved in the late-gestation decrease in gonadotrophin secretion in the ovine fetus." Proceedings of the British Society of Animal Science 1999 (1999): 66. http://dx.doi.org/10.1017/s1752756200002210.
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The mid-gestation peak in activity of the fetal gonadotrophic axis is thought to be crucial for normal reproductive development. It is clear that the increase to mid-gestation is a result of the concomitant rise in gonadotrophs (Thomas et al., 1993). The mechanisms responsible for the decrease after mid-gestation are unclear, but may involve feedback from the placental steroids (Challis et al., 1981; Gluckman et al., 1983). The aim was to determine the roles of the placental steroids, progesterone and oestradiol, in the late-gestation decline in fetal gonadotrophins using the oestradiol antagonist ICI 182,780 and the progesterone antagonist RU486.
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Themmen, Axel P. N. "An update of the pathophysiology of human gonadotrophin subunit and receptor gene mutations and polymorphisms." Reproduction 130, no. 3 (September 2005): 263–74. http://dx.doi.org/10.1530/rep.1.00663.
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New information about mutations and polymorphisms in the genes for the gonadotrophins and their receptors has become available in the last few years. In this short review mutations and polymorphisms in gonadotrophins, their receptors and their pathophysiological effects and implications are discussed. An increasingly clear picture about the structure–function relationships of gonadotrophin action is emerging from the combining the types and the locations of the mutations with their phenotypic effects and the information about the crystal structure of these molecules.
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Sutton-McDowall, Melanie L., Robert B. Gilchrist, and Jeremy G. Thompson. "Effect of hexoses and gonadotrophin supplementation on bovine oocyte nuclear maturation during in vitro maturation in a synthetic follicle fluid medium." Reproduction, Fertility and Development 17, no. 4 (2005): 407. http://dx.doi.org/10.1071/rd04135.
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In vitro oocyte maturation (IVM) culture conditions have been relatively unchanged over the past few decades and remain suboptimal. In contrast, studies of the in vivo environment have led to significant improvements to in vitro embryo culture technologies. The aim of the present study was to determine the effect of maturing bovine cumulus–oocyte complexes (COCs) in medium based on the composition of bovine follicular fluid (Bovine VitroMat; Cook Australia, Eight Mile Plain, Qld, Australia). In particular, the effect of different glucose concentrations and glucosamine supplementation on meiotic maturation was determined. Culturing COCs in the presence of gonadotrophins in Bovine VitroMat, containing either physiological glucose concentrations (2.3 mm) or 5.6 mm (equivalent to levels in Tissue Culture Medium 199 (TCM199)) supplemented with glucosamine resulted in comparable cumulus expansion to COCs cultured in TCM199 plus gonadotrophins. However, nuclear maturation was 1.3-fold lower in Bovine VitroMat cultures containing 2.3 mm glucose compared with 5.6 mm glucose and this effect was independent of glucosamine supplementation. Investigations into the effects of different glucose concentrations and gonadotrophin supplementation during the initial 6 h of maturation demonstrated that COCs cultured in Bovine VitroMat with 5.6 mm glucose without gonadotrophins had a twofold acceleration of the rate of meiotic resumption, yet the rate of polar body formation was decreased by approximately 20% compared with cultures in 2.3 mm glucose and TCM199. However, this effect was not seen when COCs were cultured for the initial 16 h in Bovine VitroMat + 5.6 mm minus gonadotrophins or in Bovine VitroMat + 2.3 mm glucose ± gonadotrophins. These data demonstrate that glucose concentrations and the timing of the introduction of gonadotrophin during IVM have variable effects on nuclear maturation. Manipulation of glucose concentrations may be a mechanism to influence oocyte meiotic progression and may lead to the development of improved IVM systems, allowing for an increased developmental capacity of bovine oocytes.
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Hutka, Marsida, Prashant Kadam, Dorien Van Saen, Natalie Z. M. Homer, Jaime Onofre, W. Hamish B. Wallace, Lee B. Smith, Jan-Bernd Stukenborg, Ellen Goossens, and Rod T. Mitchell. "Fertility Preservation in Childhood Cancer: Endocrine Activity in Prepubertal Human Testis Xenografts Exposed to a Pubertal Hormone Environment." Cancers 12, no. 10 (September 30, 2020): 2830. http://dx.doi.org/10.3390/cancers12102830.
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Survivors of childhood cancer are at risk for long-term treatment-induced health sequelae, including gonadotoxicity and iatrogenic infertility. At present, for prepubertal boys there are no viable clinical options to preserve future reproductive potential. We investigated the effect of a pubertal induction regimen with gonadotrophins on prepubertal human testis xenograft development. Human testis tissue was obtained from patients with cancer and non-malignant haematological disorders (n = 6; aged 1–14 years) who underwent testis tissue cryopreservation for fertility preservation. Fresh and frozen-thawed testis fragments were transplanted subcutaneously or intratesticularly into immunocompromised mice. Graft-bearing mice received injections of vehicle or exogenous gonadotrophins, human chorionic gonadotrophin (hCG, 20 IU), and follicle-stimulating hormone (FSH, 12.5 IU) three times a week for 12 weeks. The gross morphology of vehicle and gonadotrophin-exposed grafts was similar for both transplantation sites. Exposure of prepubertal human testis tissue xenografts to exogenous gonadotrophins resulted in limited endocrine function of grafts, as demonstrated by the occasional expression of the steroidogenic cholesterol side-chain cleavage enzyme (CYP11A1). Plasma testosterone concentrations (0.13 vs. 0.25 ng/mL; p = 0.594) and seminal vesicle weights (10.02 vs. 13.93 mg; p = 0.431) in gonadotrophin-exposed recipient mice were comparable to vehicle-exposed controls. Regardless of the transplantation site and treatment, initiation and maintenance of androgen receptor (AR) expression were observed in Sertoli cells, indicating commitment towards a more differentiated status. However, neither exogenous gonadotrophins (in castrated host mice) nor endogenous testosterone (in intact host mice) were sufficient to repress the expression of markers associated with immature Sertoli cells, such as anti-Müllerian hormone (AMH) and Ki67, or to induce the redistribution of junctional proteins (connexin 43, CX43; claudin 11, CLDN11) to areas adjacent to the basement membrane. Spermatogonia did not progress developmentally but remained the most advanced germ cell type in testis xenografts. Overall, these findings demonstrate that exogenous gonadotrophins promote partial activation and maturation of the somatic environment in prepubertal testis xenografts. However, alternative hormone regimens or additional factors for pubertal induction are required to complete the functional maturation of the spermatogonial stem cell (SSC) niche.
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Johnson, M. S., R. Mitchell, and G. Fink. "The role of protein kinase C in LHRH-induced LH and FSH release and LHRH self-priming in rat anterior pituitary glands in vitro." Journal of Endocrinology 116, no. 2 (February 1988): 231–39. http://dx.doi.org/10.1677/joe.0.1160231.
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ABSTRACT We have investigated the role of protein kinase C (PKC) in LHRH-induced LH and FSH secretion and LHRH priming. Hemipituitary glands from pro-oestrous rats were incubated with agents known to affect PKC and with or without LHRH, during which time the secretion of gonadotrophins was measured. Phorbol esters and phospholipase C, activators of PKC, released LH and FSH in a concentration-dependent manner and potentiated the LHRH-induced secretion of gonadotrophins in parallel with their ability to release these hormones alone. Inhibitors of PKC had either no effect on LH release (1-(5-isoquinolinesulphonyl)-2-methylpiperazine hydrochloride) or they augmented LHRH-induced gonadotrophin release (polymyxin B and 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate). Neither the activators nor the inhibitors of PKC, when present with LHRH, caused any change in LHRH priming, even though the activators alone produced a release of gonadotrophins that showed a temporal pattern similar to that produced by LHRH priming. The profiles of effects on LH and FSH secretion were always qualitatively similar. These results show that PKC may be involved in general regulation of gonadotrophin release but that it is not important in acute responses to LHRH nor in LHRH self-priming. J. Endocr. (1988) 116, 231–239
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&NA;. "Gonadotrophins." Reactions Weekly &NA;, no. 564 (August 1995): 8. http://dx.doi.org/10.2165/00128415-199505640-00021.
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&NA;. "Gonadotrophins." Reactions Weekly &NA;, no. 636 (February 1997): 8. http://dx.doi.org/10.2165/00128415-199706360-00028.
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Matorras, R. "Prions, urinary gonadotrophins and recombinant gonadotrophins." Human Reproduction 18, no. 5 (May 1, 2003): 1129–30. http://dx.doi.org/10.1093/humrep/deg176.
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Einspanier, A., and J. K. Hodges. "LH- and chorionic gonadotrophin-stimulated progesterone release in vitro by intact luteal tissue of the marmoset monkey (Callithrix jacchus)." Journal of Endocrinology 141, no. 3 (June 1994): 403–9. http://dx.doi.org/10.1677/joe.0.1410403.
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Abstract The application of an in vitro microdialysis system (MDS) for studies on the gonadotrophic control of luteal progesterone secretion in the marmoset monkey is described. Luteal tissue collected from a total of six animals (9 ± 1 days after ovulation) was perfused with Ringer solution (without and with lipoprotein, 0·6 μg/ml). The tissue was exposed to repeated applications of human LH (hLH) and human chorionic gonadotrophin (hCG) (1, 10 and 100 IU/ml) each of 60 min duration. Perfusate was collected in 15-min fractions and assayed for progesterone content. Results showed that addition of lipoproteins to the Ringer solution had a marked effect on progesterone secretion in terms of maintaining stable baseline levels and improving reproducibility of gonadotrophin-induced responses. Progesterone secretion was significantly stimulated by both gonadotrophins at each dose tested. Maximal elevations were obtained with 10 IU/ml and there were no apparent differences in responses to hLH and hCG in terms of either magnitude or duration. This study indicates that MDS provides a useful in vitro approach for studying the gonadotrophic control of the corpus luteum in non-human primates. The results did not demonstrate disparate actions of hLH and hCG in their ability to stimulate luteal progesterone secretion. Journal of Endocrinology (1994) 141, 403–409
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Kobayashi, M., R. Nakano, and A. Ooshima. "Immunohistochemical localization of pituitary gonadotrophins and gonadal steroids confirms the 'two-cell, two-gonadotrophin' hypothesis of steroidogenesis in the human ovary." Journal of Endocrinology 126, no. 3 (September 1990): 483—NP. http://dx.doi.org/10.1677/joe.0.1260483.
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ABSTRACT Ovaries from 37 women with normal menstrual cycles were analysed for localization of pituitary gonadotrophins and gonadal steroids using an immunohistochemical method. In the follicular phase, FSH and oestradiol-17β localized in the granulosa layer, and LH, progesterone and testosterone localized in the internal thecal layer. In the luteal phase, gonadotrophins and steroids localized in luteal cells. Particularly in the early luteal phase, FSH and oestradiol-17β localized in large luteal cells, and LH, progesterone and testosterone localized in small luteal cells. The results of the present immunohistochemical analysis confirm the two-cell, two-gonadotrophin hypothesis of steroidogenesis in the human ovary. Journal of Endocrinology (1990) 126, 483–488
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Kaneko, Hiroyuki, Kazuhiro Kikuchi, Junko Noguchi, Manabu Ozawa, Katsuhiko Ohnuma, Naoki Maedomari, and Naomi Kashiwazaki. "Effects of gonadotrophin treatments on meiotic and developmental competence of oocytes in porcine primordial follicles following xenografting to nude mice." Reproduction 131, no. 2 (February 2006): 279–88. http://dx.doi.org/10.1530/rep.1.00957.
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Our objective was to improve the developmental ability of oocytes in porcine primordial follicles xenografted to nude mice, by treating the host mice with gonadotrophins to accelerate follicular growth. Ovarian tissues from 20-day-old piglets, in which most of the follicles were primordial, were transplanted under the kidney capsules of ovariectomized nude mice. Gonadotrophin treatments were commenced around 60 days after vaginal cornification in the mice. Ovarian grafts were obtained 2 or 3 days after treatment with equine chorionic gonadotrophin (eCG-2 and eCG-3 groups), after porcine FSH infusion for 7 or 14 days, or after infusion of porcine FSH for 14 days with a single injection of estradiol antiserum (FSH-7, FSH-14 and FSH-14EA groups, respectively). Gonadotrophin treatments accelerated follicular growth within the xenografts compared with that in control mice given no gonadotrophins, consistent with higher (P < 0.05) circulating inhibin levels in the gonadotrophin-treated mice. In contrast, circulating mouse FSH levels were significantly (P < 0.05) depressed. We recovered large numbers of full-sized oocytes with meiotic competence to the mature stage from the eCG-3, FSH-7, and FSH-14EA, unlike in the control group. Moreover, 56% of matured oocytes with the first polar body (n = 39) were fertilized in vitro in the FSH-14EA group. After in vitro fertilization and subsequent culture for 7 days, one blastocyst was obtained from each of the eCG-3, FSH-7 and, FSH-14EA groups, whereas no blastocysts appeared in the other groups. Exogenous gonadotrophins –not mouse FSH – stimulated the growing follicles that had developed from the primordial follicles in the xenografts: the effects were incomplete but improved to some extent the meiotic and developmental abilities of the oocytes.
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Jonas, Kim C., Olayiwola O. Oduwole, Hellevi Peltoketo, Susana B. Rulli, and Ilpo T. Huhtaniemi. "Mouse models of altered gonadotrophin action: insight into male reproductive disorders." REPRODUCTION 148, no. 4 (October 2014): R63—R70. http://dx.doi.org/10.1530/rep-14-0302.
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The advent of technologies to genetically manipulate the mouse genome has revolutionised research approaches, providing a unique platform to study the causality of reproductive disorders in vivo. With the relative ease of generating genetically modified (GM) mouse models, the last two decades have yielded multiple loss-of-function and gain-of-function mutation mouse models to explore the role of gonadotrophins and their receptors in reproductive pathologies. This work has provided key insights into the molecular mechanisms underlying reproductive disorders with altered gonadotrophin action, revealing the fundamental roles of these pituitary hormones and their receptors in the hypothalamic–pituitary–gonadal axis. This review will describe GM mouse models of gonadotrophins and their receptors with enhanced or diminished actions, specifically focusing on the male. We will discuss the mechanistic insights gained from these models into male reproductive disorders, and the relationship and understanding provided into male human reproductive disorders originating from altered gonadotrophin action.
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Pinilla, L., P. Garnelo, M. Tena-Sempere, F. Gaytan, and E. Aguilar. "Mechanisms of reproductive deficiency in male rats treated neonatally with a gonadotrophin-releasing hormone antagonist." Journal of Endocrinology 142, no. 3 (September 1994): 517–25. http://dx.doi.org/10.1677/joe.0.1420517.
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Abstract It is well known that males injected neonatally with oestradiol or antiserum or antagonists (ANT) against gonadotrophin-releasing hormone (GnRH) show multiple reproductive disorders. In the present work, in males treated neonatally with GnRH-ANT, we have analysed: (1) whether the impairment of reproductive function can be blocked by simultaneous treatment with gonadotrophins, (2) the possible differences in the effects of GnRH-ANT injected before or after the proliferation of Sertoli cells which takes place between days 1 and 15 of age, and (3) the mechanism(s) for the increased FSH secretion observed in adulthood. Experimental designs included: administration of GnRH-ANT between days 1 and 16 or 15 and 30 of age, simultaneous administration of gonadotrophins and GnRH-ANT to neonatal males, and measurement of FSH secretion after orchidectomy or specific destruction of Leydig cells with ethylene dimethane sulphonate (EDS) in adult males treated neonatally with GnRH-ANT. The principal new data presented in our studies are the following: (1) delayed puberty was observed not only in males injected neonatally with GnRH-ANT, but also in those injected with gonadotrophins or with GnRH-ANT and gonadotrophins, (2) the decreased fertility and increased FSH secretion observed in adult males treated neonatally with GnRH-ANT were normalized by simultaneous administration of GnRH-ANT and gonadotrophins, and (3) the increased FSH secretion in adult males treated neonatally with GnRH-ANT remained after EDS or orchidectomy, suggesting that mechanisms other than decreased inhibin secretion were involved in the increased secretion of FSH. Journal of Endocrinology (1994) 142, 517–525
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Kotsuji, F., K. Hosokawa, and T. Tominaga. "Daily administration of gonadotrophin-releasing hormone increases pituitary gonadotroph number and pituitary gonadotrophin content, but not serum gonadotrophin levels, in female rats on day 1 of dioestrus." Journal of Endocrinology 132, no. 3 (March 1992): 395—NP. http://dx.doi.org/10.1677/joe.0.1320395.
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ABSTRACT Gonadotrophin-releasing hormone (GnRH) has been shown to regulate the synthesis and release of gonadotrophins acutely, yet few studies have investigated the chronic effects of this agent on pituitary gonadotrophins. In the present study we determined the effect of chronic administration of GnRH on the female rat pituitary gland. Rats of 8 weeks of age were injected s.c. with various doses of GnRH daily for 30 days. After completion of the GnRH treatment, treated rats and age-matched controls were killed by decapitation at 09.00 h on the first day of dioestrus, as determined from vaginal smears. Treatment with 10 ng–10 μg GnRH/day increased pituitary contents of FSH and LH in a dose-dependent manner. The change in FSH content was much greater than that of LH content. The pituitary FSH content of rats treated with 40 μg GnRH was significantly less than that of rats treated with 10 μg GnRH. There was a marked increase in the number of cells which stained positively for FSH (266%) and LH (28%) in the anterior pituitary of rats given 10 μg GnRH, but there was no demonstrable change in the areas of single cells stained positively for FSH and LH. Serum levels of LH, FSH and oestradiol were not affected by the GnRH treatment. These data indicate that chronic administration of GnRH is capable of increasing the pituitary gonadotrophin content and numbers of FSH and/or LH-stained cells and that FSH cells are affected more than LH cells by the GnRH treatment. The increase in pituitary gonadotrophin content, however, does not necessarily produce an increase in circulating levels of gonadotrophins. Journal of Endocrinology (1992) 132, 395–400
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Meijs-Roelofs, H. M. A., W. A. van Cappellen, E. C. M. van Leeuwen, and P. Kramer. "Short- and long-term effects of an LHRH antagonist given during the prepubertal period on follicle dynamics in the rat." Journal of Endocrinology 124, no. 2 (February 1990): 247–53. http://dx.doi.org/10.1677/joe.0.1240247.
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ABSTRACT The effects of the suppression of the high gonadotrophin concentrations normally present by the end of the second week of life on ovarian follicle dynamics were studied in immature rats. Gonadotrophins were suppressed by treatment with an LHRH antagonist (LHRH-A; Org. 30276) on days 6, 9, 12 and 15, and the total population of ovarian follicles was studied at 15 and 28 days, on the day of first oestrus and on the day of oestrus at or following 90 and 300 days of age. Primordial follicles were counted and growing follicles were counted and measured. In rats treated with LHRH-A, follicle recruitment into the growing pool was clearly diminished; the number of growing follicles was significantly (P<0·01) lower up to the day of first oestrus and the pool of primordial follicles was significantly (P<0·05) larger at 15 and 28 days. Ovarian weights were significantly lower in rats treated with LHRH-A until at least 90 days of age. However, on the day of oestrus at or after 90 and 300 days of age, there were no differences in either the pool of primordial follicles or the pool of growing follicles between rats treated with LHRH-A and control rats. There was also no difference between groups in the number of fresh corpora lutea at these ages. It was concluded that the early peak in gonadotrophin concentrations in immature rats causes substantial recruitment of follicles into the growing pool. Thus, the number of follicles entering the growing pool is not solely dependent upon the size of the pool of primordial follicles but is clearly influenced by the level of circulating gonadotrophins. In contrast, the large gonadotrophic stimulation that normally takes place during the second and third week of life is neither a prerequisite for functional sexual maturation nor for later cyclic function. Shortly before the time of first ovulation a tight control of follicle dynamics is established which is largely independent of previous gonadotrophin concentrations and follicle dynamics. Journal of Endocrinology (1990) 124, 247–253
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Gray, S. A., M. A. Mannan, and P. J. O'Shaughnessy. "Development of cytochrome P450 17α-hydroxylase (P450c17) mRNA and enzyme activity in neonatal ovaries of normal and hypogonadal (hpg) mice." Journal of Molecular Endocrinology 17, no. 1 (August 1996): 55–60. http://dx.doi.org/10.1677/jme.0.0170055.
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ABSTRACT The cytochrome P450 enzyme 17α-hydroxylase (P450c17) is required for androgen synthesis and therefore regulates substrate supply for aromatization. In this study, changes in P450c17 activity and mRNA levels were measured during ovarian development in the normal mouse and in the hypogonadal (hpg) mouse which lacks circulating gonadotrophins. At birth, low levels of P450c17 activity and mRNA were detectable in normal ovaries. This basal level of expression did not change until after day 10 at which time both enzyme activity and mRNA levels increased by six- to eightfold. In the hpg mouse, levels of P450c17 mRNA were normal at birth but did not change significantly during subsequent development and were significantly less than normal by day 15. Results show that there is a low level of gonadotrophin-independent expression of P450c17 in the ovary at birth and that gonadotrophins are required for the subsequent increase in expression between days 10 and 15. In the ovary, P450c17 is expressed solely in the thecal/interstitial compartment and interstitial cells arise in the mouse ovary around day 11. Changes in P450c17 are likely, therefore, to be related to gonadotrophin-dependent development of the interstitial tissue in the mouse. Treatment of adult hpg mice with LH and FSH showed that both gonadotrophins can act to increase P450c17 activity. Since FSH acts only on the granulosa cell compartment of the ovary it is likely that FSH acts through a paracrine mechanism to regulate thecal/interstitial cell activity.
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Nagahara, Yasuhito, Akira Miyake, Keiichi Tasaka, Yasuhiro Kawamura, Toshihiro Aono, and Osamu Tanizawa. "Possible site of negative and positive feedback action of oestrogen on gonadotrophin secretion in normal women." Acta Endocrinologica 108, no. 4 (April 1985): 440–44. http://dx.doi.org/10.1530/acta.0.1080440.
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Abstract. For determination of the site of action of oestrogen (E) during the negative and positive feedback phases of gonadotrophin secretions, studies were made on the pituitary response to a small amount of LRH and the pulsatility of gonadotrophins after E administration in normal cycling women in the mid-follicular phase. The pituitary responses to an iv bolus of 2.5 μg of synthetic LRH were evaluated by measuring serum LH and FSH 2 h before and 8 h after administration of 20 mg of conjugated E (Premarin). In the next cycle, the pituitary responses to a same dose of LRH were also observed 2 h before and 56 h after E injection. The mean levels of serum LH and FSH and the peak responses to LRH were significantly (P < 0.05) decreased 8 h after E injection, but were significantly (P < 0.05) increased 56 h after E administration. In the third cycle, the pulsatility of gonadotrophins was evaluated by measuring serum LH and FSH every 15 min for 180 min before and 8 h and 56 h after E injection. The pulse frequencies of gonadotrophins were not significantly different before and 8 h and 56 h after E injection. The amplitudes of pulses 56 h after Premarin injection were significantly higher than those before the injection. These findings suggest that the negative and positive feedback effects of E on gonadotrophin secretion may be caused, in part, by its direct action on the pituitary response to LRH.
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Wilson, C. A., A. J. Leigh, and A. J. Chapman. "Gonadotrophin glycosylation and function." Journal of Endocrinology 125, no. 1 (April 1990): 3–14. http://dx.doi.org/10.1677/joe.0.1250003.
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ABSTRACT This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat. In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone. Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation. Journal of Endocrinology (1990) 125, 3–14
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Scaramuzzi, RJ, NR Adams, DT Baird, BK Campbell, JA Downing, JK Findlay, KM Henderson, et al. "A model for follicle selection and the determination of ovulation rate in the ewe." Reproduction, Fertility and Development 5, no. 5 (1993): 459. http://dx.doi.org/10.1071/rd9930459.
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A model for folliculogenesis is proposed that is based as far as possible on a knowledge of physiological, rather than anatomical, changes taking place during follicle development. The model is therefore functional, rather than descriptive, and consists of five classes of follicles that have been defined by their dependency and sensitivity to gonadotrophins. These classes are: primordial, committed, gonadotrophin-responsive, gonadotrophin-dependent and ovulatory. The model is an attempt to encourage discussion and to promote the integration of morphological models of folliculogenesis with recent advances in the molecular endocrinology of the ovarian follicle. Two hypotheses for the mechanisms that determine ovulation rate are developed in light of the model. In the first, multiple ovulation results when the viability of gonadotropin-dependent follicles is enhanced. In the second, multiple ovulation is caused by increasing the number of gonadotrophin-responsive follicles available for further development; this results from the increasing rate of folliculogenesis and the throughput of follicles. The final section of this paper examines how these two hypothetical mechanisms, which are not mutually exclusive, appear to account for most of the known genetical and environmental effects on ovulation rate of sheep. In particular, the effects of nutrition, genotype, exogenous gonadotrophins, immunity to both oestrogens and androgens, and immunity to inhibin are discussed.
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Ulloa-Aguirre, Alfredo, and Carlos Timossi. "Biochemical and functional aspects of gonadotrophin-releasing hormone and gonadotrophins." Reproductive BioMedicine Online 1, no. 2 (January 2000): 48–62. http://dx.doi.org/10.1016/s1472-6483(10)61901-3.
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Tortonese, Domingo J., Susan J. Gregory, Rebecca C. Eagle, Carolyne L. Sneddon, Claire L. Young, and Julie Townsend. "The equine hypophysis: a gland for all seasons." Reproduction, Fertility and Development 13, no. 8 (2001): 591. http://dx.doi.org/10.1071/rd01066.
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The intrahypophysial mechanisms involved in the control of gonadotrophin secretion remain unclear. In the horse, a divergent pattern of gonadotrophins is observed at different stages of the reproductive cycle in response to a single secretagogue (gonadotrophin-releasing hormone), and dramatic changes in fertility take place throughout the year in response to photoperiod. This species thus provides a useful model to investigate the regulation of fertility directly at the level of the hypophysis. A series of studies were undertaken to examine the cytological arrangements and heterogeneity of gonadotrophin storage in the pars distalis (PD) and pars tuberalis (PT) of the hypophysis of male and female horses. Specifically, the seasonal and gonadal effects on distribution, density and hormonal identity of gonadotrophs, the existence of gonadotroph–lactotroph associations and the expression of prolactin receptors (PRL-R) as possible morphological bases for the differential control of gonadotrophin secretion were investigated. It became apparent that both isolated and clustered gonadotrophs are normally distributed around the pars intermedia and surrounding capillaries in the PD, and in the caudal ventral region of the PT. In the PD, no effects of season or of reproductive state on the density or number of gonadotrophs could be detected in either male or female animals. In contrast, a fivefold increase in gonadotroph density was observed in the PT during the sexually active stage. In males, robust gonadal effects were detected on the gonadotroph population; orchidectomy significantly reduced both the number and proportion of gonadotrophs, in relation to other hypophysial cell types, in both the PD and PT regions. Luteinizing hormone (LH) monohormonal, follicle-stimulating hormone (FSH) monohormonal and bihormonal gonadotrophs were identified in the PD and PT of male and female horses. Interestingly, in males, the relative proportions of gonadotroph subtypes and the LH/FSH monohormonal gonadotroph ratio were not affected by either season or the presence of the gonads. In contrast, a larger proportion of monohormonal gonadotrophs was clearly observed in sexually active females. Specific gonadotroph–lactotroph associations and expression of PRL-R in cells other than gonadotrophs were detected in the PD throughout the annual reproductive cycle. In addition to a stimulatory gonadal effect on lactotroph density, a substantial gonadal-independent effect of season was apparent on this variable. The findings have revealed important seasonal and gonadal effects on the cytological configuration of the equine hypophysis, which may provide the morphological basis for the intrahypophysial control of fertility.
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Hayden, Catherine J., Adam H. Balen, and Anthony J. Rutherford. "Recombinant gonadotrophins." BJOG: An International Journal of Obstetrics and Gynaecology 106, no. 3 (March 1999): 188–96. http://dx.doi.org/10.1111/j.1471-0528.1999.tb08230.x.
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Thomas, G. B., A. S. McNeilly, F. Gibson, and A. N. Brooks. "Effects of pituitary-gonadal suppression with a gonadotrophin-releasing hormone agonist on fetal gonadotrophin secretion, fetal gonadal development and maternal steroid secretion in the sheep." Journal of Endocrinology 141, no. 2 (May 1994): 317–24. http://dx.doi.org/10.1677/joe.0.1410317.
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Abstract In order to investigate the regulation of the hypothalamo-pituitary-gonadal axis during fetal development, sheep fetuses at day 70 of gestation were implanted subcutaneously with a biodegradable implant containing the longacting gonadotrophin-releasing hormone (GnRH) agonist, buserelin. The treatment of fetuses with a GnRH agonist throughout the last half of gestation (term=145 days) abolished the increase in plasma LH concentrations that was seen in 2-day-old control lambs in response to an injection of GnRH. This attenuated response was associated with corresponding reductions in the pituitary content of LH and FSH. Immunolocalization studies revealed that pituitary glands from newborn lambs implanted with a GnRH agonist during fetal development were devoid of immunopositive LH- and FSH-containing cells. At birth the testicular weights of GnRH agonist-treated ram lambs were significantly decreased by 40% when compared with controls. This was associated with a 45% reduction in the total number of Sertoli cells per testis. In newborn ewe lambs GnRH agonist treatment had no effect on ovarian weight or on the morphological appearance of the ovaries. GnRH agonist treatment had no effect on the plasma concentrations of progesterone and oestrone in the maternal circulation or on the length of gestation. These results show (1) that GnRH positively regulates the synthesis and secretion of gonadotrophins in the fetus, (2) that reduced fetal gonadotrophic support during the last half of gestation results in a reduction in testicular growth, and (3) that fetal gonadotrophins do not affect maternal steroid secretion. Journal of Endocrinology (1994) 141, 317–324
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Juengel, Jennifer L., Laurel D. Quirke, Stan Lun, Derek A. Heath, Peter D. Johnstone, and Kenneth P. McNatty. "Effects of immunizing ewes against bone morphogenetic protein 15 on their responses to exogenous gonadotrophins to induce multiple ovulations." REPRODUCTION 142, no. 4 (October 2011): 565–72. http://dx.doi.org/10.1530/rep-11-0126.
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Sheep with a heterozygous inactivating mutation in the bone morphogenetic protein 15 (BMP15) gene experience an increased ovulation rate during either a natural oestrous cycle or a cycle in which exogenous FSH and eCG (gonadotrophins) are given to induce multiple ovulations. The primary aim of these studies was to determine whether ewes immunised against BMP15 would also show an improved superovulation rate following exogenous gonadotrophin treatment. A secondary aim was to determine the effects of BMP15 immunisation on ovarian follicular characteristics. In most ewes (i.e. >75%) immunised with a BMP15-keyhole limpet haemocyanin peptide in an oil-based adjuvant in order to completely neutralise BMP15 bioactivity, there was no superovulation response to exogenous gonadotrophins. In ewes treated with exogenous gonadotrophins following a BMP15-BSA peptide immunisation in a water-based adjuvant to partially neutralise BMP15 bioactivity, the ovulation rate response was similar to the control superovulation treatment groups. Characterisation of follicular function revealed that the water-based BMP15-immunised animals had fewer non-atretic follicles 2.5–3.5 or >4.5 mm in diameter compared with controls. Basal concentrations of cAMP were higher in granulosa cells from animals immunised against BMP15 than control animals. There were no significant differences in the concentrations of cAMP between granulosa cells from BMP15- and control-immunised animals when given FSH or hCG, although there were differences in the proportions of follicles in different size classes that responded to FSH or hCG. Thus, immunisation against BMP15 may have been causing premature luteinisation and thereby limiting the numbers of follicles recruited for ovulation following treatment with exogenous gonadotrophins.
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Crosier, Adrienne E., Pierre Comizzoli, Diana C. Koester, and David E. Wildt. "Circumventing the natural, frequent oestrogen waves of the female cheetah (Acinonyx jubatus) using oral progestin (Altrenogest)." Reproduction, Fertility and Development 29, no. 8 (2017): 1486. http://dx.doi.org/10.1071/rd16007.
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Cheetah are induced ovulators, experiencing short, variable oestrogen waves year-round. Exogenous gonadotrophin administration induces ovulation, but success is variable and often improves if ovaries are quiescent. After affirming the presence of short-term oestrogenic waves, we examined the effect of the timing of administration of exogenous equine and human chorionic gonadotrophins (eCG–hCG) within the oestrogen concentration pattern on subsequent follicle development and oocyte and corpus luteum quality. We also investigated ovarian suppression using an oral progestin (Altrenogest, 7 days) and assessed whether Altrenogest moderated adrenal activity by reducing glucocorticoid metabolites. All cheetahs exhibited short (every ~7–10 days), sporadic, year-round increases in faecal oestradiol punctuated by unpredictable periods (4–10 weeks) of baseline oestradiol (anoestrous). Gonadotrophin (eCG–hCG) efficacy was not affected by oestradiol ‘wave’ pattern if administered ≥3 days after an oestrogen peak. Such cheetahs produced normative faecal progestagen patterns and higher numbers (P < 0.06) of mature oocytes than females given gonadotrophins ≤2 days after an oestradiol peak. Altrenogest supplementation expanded the interval between oestradiol peaks to 12.9 days compared with 7.3 days without progestin pretreatment. Altrenogest-fed females excreted less (P < 0.05) glucocorticoid metabolites than non-supplemented counterparts. Results show that Altrenogest is effective for suppressing follicular activity, may contribute to reduced glucocorticoid production and may result in more effective ovulation induction via gonadotrophin therapy.
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Chopineau, M., N. Martinat, H. Marichatou, C. Troispoux, C. Auge-Gouillou, F. Stewart, Y. Combarnous, and F. Guillou. "Evidence that the alpha-subunit influences the specificity of receptor binding of the equine gonadotrophins." Journal of Endocrinology 155, no. 2 (November 1, 1997): 241–45. http://dx.doi.org/10.1677/joe.0.1550241.
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Horse LH/chorionic gonadotrophin (eLH/CG) exhibits, in addition to its normal LH activity, a high FSH activity in all other species tested. Donkey LH/CG (dkLH/CG) also exhibits FSH activity in other species, but about ten times less than the horse hormone. In order to understand the molecular basis of these dual gonadotrophic activities of eLH/CG and dkLH/CG better, we expressed, in COS-7 cells, hybrids between horse and donkey subunits, between horse or donkey alpha-subunit and human CG beta (hCG beta), and also between the porcine alpha-subunit and horse or donkey LH/CG beta. The resultant recombinant hybrid hormones were measured using specific FSH and LH in vitro bioassays which give an accurate measure of receptor binding specificity and activation. Results showed that it is the beta-subunit that determines the level of FSH activity, in agreement with the belief that it is the beta-subunit which determines the specificity of action of the gonadotrophins. However, donkey LH/CG beta combined with a porcine alpha-subunit exhibited no FSH activity although it showed full LH activity. Moreover, the hybrid between horse or donkey alpha-subunit and hCG beta also exhibited only LH activity. Thus, the low FSH activity of dkLH/CG requires an equine (donkey or horse) alpha-subunit combined with dkLH/CG beta. These results provide the first evidence that an alpha-subunit can influence the specificity of action of a gonadotrophic hormone.
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Angervo, M., R. Koistinen, and M. Seppälä. "Epidermal growth factor stimulates production of insulin-like growth factor-binding protein-1 in human granulosa-luteal cells." Journal of Endocrinology 134, no. 1 (July 1992): 127–31. http://dx.doi.org/10.1677/joe.0.1340127.
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ABSTRACT Insulin-like growth factor-I (IGF-I) enhances and epidermal growth factor (EGF) inhibits gonadotrophin-induced aromatization in granulosa cells. Our previous studies have shown that human ovarian granulosa cells synthesize insulin-like growth factor-binding protein-1 (IGFBP-1) which inhibits IGF-stimulated DNA synthesis. The present study addresses the effect of EGF and gonadotrophins in the regulation of IGFBP-1 release by human granulosa cells cultured in serum-free medium. At concentrations of 1–100 μg/l EGF was found to stimulate IGFBP-1 secretion. This was not due to cell proliferation, as the viable cell count remained unaffected. Growth hormone and gonadotrophins had no effect on IGFBP-1 secretion when added alone to culture medium. These results suggest that EGF regulates IGFBP-1 secretion in human granulosa-luteal cells. Journal of Endocrinology (1992) 134, 127–131
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Peltoketo, H., A. Rivero-Müller, P. Ahtiainen, M. Poutanen, and I. Huhtaniemi. "Consequences of genetic manipulations of gonadotrophins and gonadotrophin receptors in mice." Annales d'Endocrinologie 71, no. 3 (May 2010): 170–76. http://dx.doi.org/10.1016/j.ando.2010.02.022.
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Chatterjee, S., A. Ray, S. Ghosh, K. Bhattacharya, A. Pakrashi, and C. Deb. "Effect of aldrin on spermatogenesis, plasma gonadotrophins and testosterone, and testicular testosterone in the rat." Journal of Endocrinology 119, no. 1 (October 1988): 75–81. http://dx.doi.org/10.1677/joe.0.1190075.
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ABSTRACT Quantitative evaluation of the different varieties of germ cells at stage VII of the seminiferous epithelium cycle, namely type-A spermatogonia (ASg), preleptotene spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc) and step 7 spermatids (7Sd), along with radioimmunoassay of plasma gonadotrophins (FSH and LH), testosterone and testicular testosterone were performed in Wistar rats following treatment with aldrin (polycyclic chlorinated hydrocarbon insecticide) for approximately one (13 days) or two cycles (26 days) of the seminiferous epithelium. Extensive degeneration of all varieties of germ cells at stage VII, reduction in the sperm count and significant reductions in plasma concentrations of LH and testosterone were observed following aldrin treatment. The reduction in plasma concentrations of FSH was statistically significant only after treatment for two cycles. The inhibitory effect of aldrin on plasma gonadotrophins, testosterone levels, testicular testosterone content and numbers of 7Sd and ASg was maximum after treatment for two cycles. Administration of human chorionic gonadotrophin along with aldrin treatment for two cycles partially prevented the degeneration of germ cells and enhanced testosterone production. The results indicate that aldrin may have a direct inhibitory influence on gonadotrophin release, but the possibility of a direct action of the insecticide at the level of the testes is also discussed. J. Endocr. (1988) 119, 75–81
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Stewart, F., J. A. Thomson, S. E. A. Leigh, and J. M. Warwick. "Nucleotide (cDNA) sequence encoding the horse gonadotrophin α-subunit." Journal of Endocrinology 115, no. 2 (November 1987): 341–46. http://dx.doi.org/10.1677/joe.0.1150341.
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ABSTRACT Several cDNA clones corresponding to mRNA for the α-subunit of the horse (Equus caballus) pituitary and placental (chorionic) gonadotrophic hormones have been isolated and sequenced. Polyadenylated mRNA was purified from horse pituitary glands (the source of FSH and LH) and horse placental tissues (the source of chorionic gonadotrophin; CG). The mRNA preparations were characterized by in-vitro translation and Northern hybridization techniques using human and ovine gonadotrophin cDNA clones as probes. Complementary DNA libraries were created from the pituitary and placental mRNAs and a human CG α-subunit probe was used to isolate several horse α-subunit cDNA clones. The α-subunit nucleotide sequence from both sources of tissue was identical, thereby indicating that in the horse (as in man) the same gonadotrophin α-subunit gene is expressed in the pituitary and placenta. Our results are consistent with transcription of a single α-subunit gene for all the glycoprotein hormones in the horse, and we suggest that the reported differences between the horse CG and FSH α-subunit amino acid sequences determined by conventional peptide sequencing methods arose due to errors in the FSH α-subunit sequence. Comparison of the deduced amino acid sequence of the horse α-subunit with that of other α-subunit sequences indicated a number of significant differences which may be related to the unusual receptor-binding properties of the equine gonadotrophins. J. Endocr. (1987) 115, 341–346
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Crawford, J. L., D. A. Heath, L. J. Haydon, B. P. Thomson, and D. C. Eckery. "Gene expression and secretion of LH and FSH in relation to gene expression of GnRH receptors in the brushtail possum (Trichosurus vulpecula) demonstrates highly conserved mechanisms." REPRODUCTION 137, no. 1 (January 2009): 129–40. http://dx.doi.org/10.1530/rep-08-0347.
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In eutherian mammals, the gonadotrophins (LH and FSH) are synthesized and stored in gonadotroph cells under the regulation of multiple mechanisms including GnRH. Very little is known about the regulation of gonadotrophin secretion and storage in pituitary glands of marsupials. This study revealed, using quantitative PCR and heterologous RIA techniques, thatLHBmRNA expression levels remained constant over the oestrous cycle, regardless of the presence of a preovulatory LH surge, which is characteristic of a hormone secreted under regulation. Our sampling regime was unable to detect pulses of LH during the follicular phase, althoughGNRHRmRNA levels had increased at this time. Pulses of LH were, however, detected in the luteal phase of cycling females, in anoestrus females and in males. There was a positive correlation between gene expression ofFSHBand plasma levels of FSH at different stages of the oestrous cycle and no pulses of FSH were detected at any time; all characteristics of a hormone secreted via the constitutive pathway. Usingin situhybridisation and immunohistochemistry methods, we determined that mRNA expression ofLHBandFSHB, and protein storage of gonadotrophins exhibited a similar pattern of localisation within the pituitary gland. Additionally, sexual dimorphism of gonadotroph populations was evident. In summary, these findings are similar to that reported in eutherians and considering that marsupial evolution diverged from eutherians over 100 million years ago suggests that the regulation of gonadotrophins is highly conserved indeed.
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Demir, Ayşe Y., Ruben EA Musson, Willem A. Schöls, and Jitze M. Duk. "Pregnancy, malignancy or mother nature? Persistence of high hCG levels in a perimenopausal woman." BMJ Case Reports 12, no. 1 (January 2019): bcr—2018–227203. http://dx.doi.org/10.1136/bcr-2018-227203.
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Despite the fact that a small percentage of peri en postmenopausal women have mild elevations in human chorionic gonadotrophin (hCG) concentrations (<14 IU/L) besides high levels of gonadotrophins, a considerable number of clinicians are not aware of this phenomenon. We report a case of a 53-year-old woman with an unusually high hCG concentration (>40 IU/L) given her menopausal state. Although a pregnancy or a malignancy was unlikely on the basis of stable hCG levels, elevated gonadotrophins and a negative transvaginal ultrasound, her physicians were uncertain and chose an expectant approach by repeated testing. Ultimately, after consulting the laboratory, analytical interference was ruled out and pituitary origin of unusual high hCG level could be confirmed after conduction of a suppression test by oestrogen–progesterone hormone replacement therapy. Until that time, the patient had undergone a vast amount of laboratory tests and gynaecology consultations, resulting in an enormous amount of confusion, anxiety and overdiagnosis.
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Khamsi, F., and S. Roberge. "Granulosa cells of the cumulus oophorus are different from mural granulosa cells in their response to gonadotrophins and IGF-I." Journal of Endocrinology 170, no. 3 (September 1, 2001): 565–73. http://dx.doi.org/10.1677/joe.0.1700565.
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There are two types of granulosa cells: those which surround the oocyte are cumulus cells (CC) and those which surround the antrum are mural granulosa cells (MGC). These cells are under the influence of several hormones and growth factors, the most important of which are gonadotrophins and IGF-I. In this article, we report novel observations on the differences between these two types of granulosa cells and their interaction with gonadotrophins and IGF-I. We were able to conduct physiological studies on the role of IGF-I by using an analogue of IGF-I which does not bind to IGF-I-binding proteins (LR3-IGF-I). Immature rats received saline, equine chorionic gonadotrophin (eCG), LR3-IGF-I or eCG plus LR3-IGF-I by infusion using a pump from 24-29 days of age. The rats were killed and the ovaries removed. Surface follicles were punctured and MGC and oocyte cumulus complexes were removed. These were cultured in saline (control) and in three different doses of FSH. Cell replication was assessed by 3H-thymidine incorporation and differentiation was evaluated by the measurement of progesterone secretion. It was noted that CC replicated ten times more than MGC. Similarly, progesterone secretion by CC was six times more than by MGC. In vivo exposure to gonadotrophins (eCG) positively influenced in vitro treatment with FSH in both cell types. This phenomenon was observed in both cell replication and progesterone secretion. The IGF-I analogue had a positive effect on cell replication of MGC but a negative effect on the cell replication of CC. With respect to progesterone secretion, the IGF-I analogue had a negative effect on CC but a positive effect on MGC. In conclusion, CC behaved differently from MGC in response to gonadotrophins and the IGF-I analogue. IGF-I and FSH acted additively, synergistically or antagonistically in different circumstances.
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Stewart, Rosemary A., Adrienne E. Crosier, Katharine M. Pelican, Budhan S. Pukazhenthi, Brandon D. Sitzmann, Tom E. Porter, David E. Wildt, Mary Ann Ottinger, and JoGayle Howard. "Progestin priming before gonadotrophin stimulation and AI improves embryo development and normalises luteal function in the cat." Reproduction, Fertility and Development 27, no. 2 (2015): 360. http://dx.doi.org/10.1071/rd13274.
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Exogenous gonadotrophins administered before AI can adversely alter endocrine dynamics and inhibit embryo development in felids. In the present study, we tested the hypothesis that priming the domestic cat ovary with progestin mitigates the negative influence of gonadotrophin therapy by normalising early embryogenesis and luteal function. Queens were given either: (1) progestin pretreatment plus chorionic gonadotrophins (n = 8; primed); or (2) gonadotrophins only (n = 8; unprimed). Ovulatory response was assessed laparoscopically, and cats with fresh corpora lutea (CL) were inseminated in utero. Ovariohysterectomy was performed 3 days later to recover intra-oviductal embryos for in vitro culture; one ovary was prepared for histology, and CL from the remaining ovary were excised and assessed for progesterone content and targeted gene expression. Of the six primed and seven unprimed queens inseminated, embryo(s) were recovered from five individuals per group. Embryos from progestin-primed donors more closely simulated normal stage in vivo development (P < 0.05). No 2- or 4-cell embryos from either group developed beyond 16-cells in vitro; however, 50% of unprimed and 66.7% of primed (P > 0.05) 5–16-cell embryos progressed to morulae or blastocysts by Day 4 of culture. Although histological characteristics were unaffected by progestin priming (P > 0.05), luteal progesterone was unusually high (P < 0.05) in unprimed compared with primed cats (72.4 ± 5.8 vs 52.2 ± 5.5 ng mg–1, respectively). Two genes associated with progesterone biosynthesis (luteinising hormone receptor and 3β-hydroxysteroid dehydrogenase) were upregulated in unprimed versus primed individuals (P = 0.05 and P < 0.05, respectively), indicating potential mechanistic pathways for the protective influence of pre-emptive progestin treatment. Building on earlier findings that progestin priming prevents spontaneous ovulation, increases ovarian sensitivity to gonadotrophins and ensures a normative endocrine environment, the present study demonstrates that pretreatment with this steroid also benefits embryo development and normalisation of early luteal function.
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Patil, Madhuri. "Gonadotrophins: The future." Journal of Human Reproductive Sciences 7, no. 4 (2014): 236. http://dx.doi.org/10.4103/0974-1208.147490.
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Nilsson, Lars, and Lars Hamberger. "6 Human gonadotrophins." Baillière's Clinical Obstetrics and Gynaecology 4, no. 3 (September 1990): 503–18. http://dx.doi.org/10.1016/s0950-3552(05)80307-4.
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Alvarez, Gabriel Martín, María Josefina Barrios Expósito, Evelin Elia, Dante Paz, Sergio Morado, and Pablo Daniel Cetica. "Effects of gonadotrophins and insulin on glucose uptake in the porcine cumulus–oocyte complex during IVM." Reproduction, Fertility and Development 31, no. 8 (2019): 1353. http://dx.doi.org/10.1071/rd18321.
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The combination of gonadotrophins (LH and FSH) and insulin is frequently used in porcine oocyte IVM, but the individual effects of gonadotrophins and insulin have not been completely studied. The aim of this study was to investigate the mechanisms involved in glucose metabolism in the swine cumulus–oocyte complex (COC), analysing the effects of gonadotrophins (10IUmL−1 LH+10IUmL−1 FSH) and 0.4μUmL−1insulin, during 44h of IVM, on glucose transport and consumption, as well as on nuclear maturation and sperm penetration. We evaluated the effects of gonadotrophins and insulin separately or in combination on glucose consumption, membrane permeability to the glucose fluorescent analogue 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-6-deoxyglucose (6-NBDG), the presence of GLUT-4 and oocyte maturation rates, after 44h of IVM. Nuclear maturation percentages increased significantly following the addition of gonadotrophins alone or in combination with insulin to the culture medium (P<0.0001), whereas insulin alone had no effect. A significant increase was observed in sperm penetration of COCs matured with insulin, gonadotrophins or their combination (P<0.0001). However, only gonadotrophins significantly increased glucose uptake (P<0.0001). Although gonadotrophins and insulin increased GLUT-4 expression, neither modified 6-NBDG incorporation. In conclusion, gonadotrophins and insulin had different effects during IVM; although gonadotrophins increased maturation rates and glucose consumption, they had no effect on glucose transport, and insulin improved sperm penetration without affecting the parameters related to glucose utilisation. Therefore, glucose metabolism is likely to be primarily regulated by its consumption in metabolic pathways rather than by changes in membrane permeability.
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Casper, Robert F. "Are recombinant gonadotrophins safer, purer and more effective than urinary gonadotrophins?" Reproductive BioMedicine Online 11, no. 5 (January 2005): 539–40. http://dx.doi.org/10.1016/s1472-6483(10)61155-8.
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Thurston, Layla, Ali Abbara, and Waljit S. Dhillo. "Investigation and management of subfertility." Journal of Clinical Pathology 72, no. 9 (July 11, 2019): 579–87. http://dx.doi.org/10.1136/jclinpath-2018-205579.
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Subfertility affects one in seven couples and is defined as the inability to conceive after 1 year of regular unprotected intercourse. This article describes the initial clinical evaluation and investigation to guide diagnosis and management. The primary assessment of subfertility is to establish the presence of ovulation, normal uterine cavity and patent fallopian tubes in women, and normal semen parameters in men. Ovulation is supported by a history of regular menstrual cycles (21–35 days) and confirmed by a serum progesterone >30 nmol/L during the luteal phase of the menstrual cycle. Common causes of anovulation include polycystic ovary syndrome (PCOS), hypothalamic amenorrhoea (HA) and premature ovarian insufficiency (POI). Tubal patency is assessed by hysterosalpingography, hystero-contrast sonography, or more invasively by laparoscopy and dye test. The presence of clinical or biochemical hyperandrogenism, serum gonadotrophins (luteinising hormone/follicle stimulating hormone) / oestradiol, pelvic ultrasound to assess ovarian morphology / antral follicle count, can help establish the cause of anovulation. Ovulation can be restored in women with PCOS using letrozole (an aromatase inhibitor), clomifene citrate (an oestrogen antagonist) or exogenous gonadotrophin administration. If available, pulsatile gonadotrophin releasing hormone therapy is the preferred option for restoring ovulation in HA. Spermatogenesis can be induced in men with hypogonadotrophic hypogonadism with exogenous gonadotrophins. Unexplained subfertility can be treated with in vitro fertilisation after 2 years of trying to conceive. Involuntary childlessness is associated with significant psychological morbidity; hence, expert assessment and prompt treatment are necessary to support such couples.
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Schramm, RD, and BD Bavister. "Effects of gonadotrophins, growth hormone and prolactin on developmental competence of domestic cat oocytes matured in vitro." Reproduction, Fertility and Development 7, no. 5 (1995): 1061. http://dx.doi.org/10.1071/rd9951061.
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Specific aims were to (1) examine the developmental capacity of felid oocytes matured in vitro and (2) determine the effects of gonadotrophins, growth hormone and prolactin on nuclear and cytoplasmic maturation oocytes in vitro. Oocytes were obtained from excised ovaries of 21 cats, and were matured for 45-46 h in modified CMRL-1066 culture medium (1 mM glutamine, 1 mM pyruvate and 20% bovine calf serum), with one of the following: (1) gonadotrophins (1.0 micrograms mL-1 hFSH+10 micrograms mL-1 hLH), (2) gonadotrophins+10 micrograms mL-1 growth hormone, (3) gonadotrophins+10 micrograms mL-1 prolactin, or (4) no hormones. Oocytes were inseminated with ejaculated cat sperm capacitated in TALP medium. Embryos were cultured in modified CMRL-1066 medium until developmental arrest, then stained with Hoechst 33342 to assess nuclear status or cell number. Gonadotrophins enhanced (P < or = 0.05) the incidence of nuclear maturation, but neither gonadotrophins, growth hormone nor prolactin improved fertilization or developmental potential of oocytes matured in vitro. Mean percentages of mature oocytes that were fertilized and cleaved to or beyond the 2, 4, 8 and 16-cell stages were 80, 77, 66, 42 and 24%, respectively. Three embryos progressed to 40-60 cells, but none developed a blastocoel. Thus, although gonadotrophins enhance nuclear maturation of oocytes in vitro, and mature oocytes are capable of fertilization and development to the morula stage, culture with growth hormone, prolactin or gonadotrophins during maturation in vitro does not enhance developmental competence or overcome the morula-to-blastocyst-stage block in development of domestic-cat oocytes matured in vitro.
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Bergendahl, M., and I. Huhtaniemi. "The time since castration influences the effects of short-term starvation on gonadotrophin secretion in male rats." Journal of Endocrinology 143, no. 2 (November 1994): 209–19. http://dx.doi.org/10.1677/joe.0.1430209.
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Abstract Short-term starvation suppresses the pituitary-testicular function in rats, evidently through inhibition of gonadotrophin-releasing hormone (GnRH) release. However, when gonadotrophin secretion is strongly enhanced, e.g. after castration, starvation does not suppress gonadotrophins. To test whether the time since castration affects the pituitary response to starvation, adult male rats were totally deprived of food for five days (only water allowed) immediately (acute castration) or two weeks after castration (chronic castration). The pituitary contents of GnRH receptors were decreased by starvation in sham-operated animals, unaffected in acutely castrated rats, but increased in chronically castrated animals, in comparison with appropriate controls (P<0·01). Castration per se increased steady-state mRNA levels of the common α-chain and the LH and FSH β-chains in all groups studied. The only consistent effect of starvation on these parameters was the 1·7 to 2-fold increase in the pituitary content of LH β-subunit mRNA in acutely and chronically castrated rats (P<0·01). Starvation alone suppressed LH secretion, acute castration eliminated this effect, but in chronically castrated rats, the starvation effect was stimulatory. Starvation did not affect FSH secretion in sham-operated and acutely castrated rats, but after chronic castration, the effect was stimulatory. In conclusion, the overall effect of starvation on gonadotrophins shifts gradually after castration from suppression, in sham-operated rats, to stimulation, in chronically castrated animals. Parallel changes in pituitary GnRH receptors suggest similar changes in GnRH secretion. Hence, starvation has both negative and positive effects on the GnRH-gonadotrophin-axis. The negative effect is evidently androgen-dependent and dominates in testes-intact animals. After chronic castration, only the positive, non-androgen dependent, stimulatory effect remains. Journal of Endocrinology (1994) 143, 209–219
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Binelli, Mario, and Bruce D. Murphy. "Coordinated regulation of follicle development by germ and somatic cells." Reproduction, Fertility and Development 22, no. 1 (2010): 1. http://dx.doi.org/10.1071/rd09218.
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The continuum of folliculogenesis begins in the fetal ovary with the differentiation of the oogonia and their isolation within the primordial follicles. Primordial follicle activation is an enigmatic process, whereby some follicles enter the growing pool to become primary follicles, thereby embarking on an irreversible progression towards ovulation or atresia. This process is under the coordinated regulation of factors from the oocyte itself, as well as from the somatic cells of the ovary, in particular the theca and granulosa cells, which are structural components of the follicle. These two influences provide the principal stimuli for the growth of the follicle to the late preantral or early antral stage of development. The endocrine effects of the gonadotrophins FSH and LH are essential to the continued progression of the follicle and most atresia can be attributed to the failure to receive or process the gonadotrophin signals. The peri-ovulatory state has received intensive investigation recently, demonstrating a coordinated role for gonadotrophins, steroids, epidermal growth factor family proteins and prostaglandins. Thus, a complex programme of coordinated interaction of governing elements from both germ and somatic cell sources is required for successful follicle development.
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de Greef, WJ, WW de Herder, CB Lambalk, W. Klootwijk, E. Sleddens-Linkels, FH de Jong, and TJ Visser. "Evidence that the TRH-like peptide pyroglutamyl-glutamyl-prolineamide in human serum may not be secreted by the pituitary gland." Journal of Endocrinology 155, no. 2 (November 1, 1997): 393–99. http://dx.doi.org/10.1677/joe.0.1550393.
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Recent studies have revealed that TRH-like immunoreactivity (TRH-LI) in human serum is predominantly pGlu-Glu-ProNH2 (< EEP-NH2), a peptide previously found in, among others tissues, the pituitary gland of various mammalian species. In the rat pituitary, < EEP-NH2 is present in gonadotrophs and its pituitary content is regulated by gonadal steroids and gonadotrophin-releasing hormone (GnRH). Hence, we reasoned that < EEP-NH2 in human serum may also arise, at least in part, from the pituitary, and that its secretion may correlate with that of gonadotrophins. Therefore, blood was simultaneously sampled from both inferior petrosal sinuses, which are major sites of the venous drainage of the pituitary gland, and a peripheral vein from seven patients with suspected adrenocorticotrophin-secreting pituitary tumours. In addition, in six postmenopausal and six cyclic women, peripheral vein blood was collected at 10-min intervals for 6 h, then a standard 100 micrograms GnRH test was performed. In the sera, TRH-LI was estimated by RIA with antiserum 4319, which binds most tripeptides that share the N- and C-terminal amino acids with TRH (pGlu-His-ProNH2). In addition, LH and FSH were measured in these sera by RIA. In the blood samples taken at 10-min intervals, an episodic variation in serum TRH-LI was noted and pulses of TRH-LI were detected at irregular intervals (from one to six pulses per 6 h) in five postmenopausal and six cyclic women. In general, these pulses did not coincide with those of LH and FSH, suggesting that TRH-LI is not co-secreted with gonadotrophins. Moreover, unlike LH and FSH, serum TRH-LI did not increase during the menopause or after exogenous administration of GnRH. Whereas gonadotrophin concentrations were significantly greater in the inferior petrosal sinus than in peripheral serum, there were no differences in TRH-LI concentrations between these serum samples. In conclusion, serum TRH-LI in humans seems not to be regulated by gonadal steroids or GnRH. Moreover, serum derived directly from the pituitary contained no more TRH-LI than did peripheral serum, which suggests that the human pituitary gland does not secrete significant amounts of < EEP-NH2, and therefore does not contribute significantly to serum TRH-LI concentrations. Further research is required to identify the site of origin of < EEP-NH2 in human serum.