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Academic literature on the topic 'Gonadotrophin secretion'

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Published: 4 June 2021

Last updated: 10 February 2022

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Journal articles on the topic "Gonadotrophin secretion"

1

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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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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Kereilwe, Onalenna, Kiran Pandey, Vitaliano Borromeo, and Hiroya Kadokawa. "Anti-Müllerian hormone receptor type 2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion." Reproduction, Fertility and Development 30, no. 9 (2018): 1192. http://dx.doi.org/10.1071/rd17377.

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Preantral and small antral follicles may secret anti-Müllerian hormone (AMH) to control gonadotrophin secretion from ruminant gonadotrophs. The present study investigated whether the main receptor for AMH, AMH receptor type 2 (AMHR2), is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion. Expression of AMHR2 mRNA was detected in anterior pituitaries (APs) of postpubertal heifers using reverse transcription–polymerase chain reaction. An anti-AMHR2 chicken antibody was developed against the extracellular region near the N-terminus of bovine AMHR2. Western blotting using this antibody detected the expression of AMHR2 protein in APs. Immunofluorescence microscopy using the same antibody visualised colocalisation of AMHR2 with gonadotrophin-releasing hormone (GnRH) receptor on the plasma membrane of gonadotrophs. AP cells were cultured for 3.5 days and then treated with increasing concentrations (0, 1, 10, 100, or 1000 pg mL−1) of AMH. AMH (10–1000 pg mL−1) stimulated (P < 0.05) basal FSH secretion. In addition, AMH (100–1000 pg mL−1) weakly stimulated (P < 0.05) basal LH secretion. AMH (100–1000 pg mL−1) inhibited GnRH-induced FSH secretion, but not GnRH-induced LH secretion, in AP cells. In conclusion, AMHR2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion.

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4

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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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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Matson, Christine, and B. T. Donovan. "Acute effects of GnRF-induced gonadotrophin secretion upon ovarian steroid secretion in the ferret." Acta Endocrinologica 111, no. 3 (March 1986): 373–77. http://dx.doi.org/10.1530/acta.0.1110373.

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Abstract. The effects of an increase in endogenous gonadotrophin secretion on the production of oestradiol, progesterone, androstenedione and testosterone by the ovaries of anaesthetized anoestrous and oestrous ferrets were followed. Gonadotrophin secretion was enhanced by the injection of gonadotrophin releasing factor (GnRF), and serial blood samples were collected over 9 h for hormone assay. Thyrotrophic hormone releasing factor (TRF) or acetic acid were injected for control purposes. The plasma content of oestradiol in oestrous females was significantly higher than during anoestrus, but secretion of this steroid was not increased by any means. The plasma concentration of progesterone in anoestrous females was significantly higher than during oestrus. It was increased by GnRF in anoestrous ferrets and less markedly in oestrous females. The plasma concentration of androstenedione was raised by GnRF to a greater extent during anoestrus than during oestrus. Testosterone was present in higher concentration in the plasma during anoestrus than during oestrus, and the level was increased by GnRF administration. These findings indicate that the ovaries of the anoestrous ferret secrete significant quantities of steroid hormones, and that they respond readily to gonadotrophic hormone.

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Daniels, M., P. Newland, J. Dunn, P. Kendall-Taylor, and M. C. White. "Long-term effects of a gonadotrophin-releasing hormone agonist ([d-Ser(But)6]GnRH(1–9)nonapeptide-ethylamide) on gonadotrophin secretion from human pituitary gonadotroph cell adenomas in vitro." Journal of Endocrinology 118, no. 3 (September 1988): 491–96. http://dx.doi.org/10.1677/joe.0.1180491.

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ABSTRACT We have studied the effects of TRH and native gonadotrophin-releasing hormone (GnRH), and of a GnRH agonist (Buserelin; [d-Ser(But)6]GnRH(1–9) nonapeptide-ethylamide), on LH, FSH, α subunit and LH-β subunit secretion from three human gonadotrophin-secreting pituitary adenomas in dispersed cell culture. During a 24 h study, treatment with 276 nmol TRH/1 resulted in a significant (P < 0·05) stimulated release of FSH and α subunit from all three adenomas, and LH from the two adenomas secreting detectable concentrations of this glycoprotein; treatment with 85 nmol GnRH/l significantly (P < 0·05) stimulated the release of α subunit from all three, but FSH from only two and LH from only one adenoma. During a long-term 28-day study, basal FSH and α subunit concentrations were maintained, but secretion of LH, and LH-β (detectable from one tumour only), declined with time from two of the three adenomas. Addition of Buserelin to the cultures resulted in the continuous (P < 0·05) stimulation of α subunit secretion from all three adenomas, and of LH and FSH from two, whilst a transient stimulatory effect on LH and FSH secretion was seen from a third adenoma, with subsequent secretion rates declining towards control values. These data show that human gonadotrophin-secreting adenomas demonstrate variable stimulatory responses to hypothalamic TRH and GnRH, and that during chronic treatment with a GnRH agonist the anticipated desensitizing effect of the drug was not observed in two out of three adenomas studied. The mechanism for this is not clear, but such drugs are unlikely to be of therapeutic value in the management of gonadotrophin-secreting tumours. The data also suggest that GnRH and GnRH agonists have a differential effect on the in-vitro release of intact gonadotrophins and the common α subunit. J. Endocr. (1988) 118, 491–496

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Hanson, P. L., S. J. B. Aylwin, J. P. Monson, and J. M. Burrin. "FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas." European Journal of Endocrinology 152, no. 3 (March 2005): 363–70. http://dx.doi.org/10.1530/eje.1.01854.

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Objective: Non-functioning pituitary adenomas (NFPAs) are characterised by the lack of symptoms of hormone hypersecretory syndromes but in vitro studies have demonstrated that tumour cells may stain for gonadotrophins and/or their α- or β-subunits. In this study, we aimed to examine the pattern of secretion of LH and FSH from a series of pituitary adenomas cultured in vitro and where data were available to relate the results to pre-operative serum gonadotrophin levels. Methods: The in vitro secretion of LH and FSH was measured from 46 cultured NFPAs and compared with pre-operative serum gonadotrophin levels in 38 patients. Peritumorous ‘normal’ pituitary cell cultures from 20 additional pituitary tumour patients were used for comparison with the NFPA group. Results: A median pre-operative LH:FSH ratio of 0.33:1 was found in 38 patients with NFPAs. Preferential secretion of FSH was also documented from media of 46 NFPAs cultured in vitro with a median LH:FSH ratio of 0.32:1. A significant correlation (r = 0.43, P < 0.01) was observed between serum and media levels of FSH but not LH. Peritumorous ‘normal’ pituitary cells released LH and FSH in a reversed ratio (median LH:FSH ratio = 3.6:1, P < 0.01 compared with NFPAs). Conclusions: This study has evaluated pre-operative serum gonadotrophin levels and in vitro release of hormones in cultures of surgically removed tissue from patients with NFPAs. The data suggest preferential secretion of FSH occurs both in vitro and in vivo. By demonstrating that NFPAs cultured in vitro reflect the in vivo situation of preferential secretion of FSH, it may be possible in future to perform functional studies using this system to elucidate the cellular and molecular mechanisms involved in the development of an imbalance in gonadotroph cells preferentially overproducing FSH in NFPAs.

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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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Antonio, Leen, Maarten Albersen, Jaak Billen, Geert Maleux, Anne-Sophie Van Rompuy, Peter Coremans, Philippe Marcq, Niels Jørgensen, and Dirk Vanderschueren. "Testicular Vein Sampling Can Reveal Gonadotropin-Independent Unilateral Steroidogenesis Supporting Spermatogenesis." Journal of the Endocrine Society 3, no. 10 (July 30, 2019): 1881–86. http://dx.doi.org/10.1210/js.2019-00180.

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Abstract Suppressed gonadotropins combined with high-normal serum testosterone concentrations in oligozoospermic men suggest either use of exogenous testosterone or presence of a testosterone-producing tumor. We describe the case of a 31-year-old man referred for primary infertility. Gonadotropins were undetectably low, but testosterone and estradiol were in the high-normal range. Semen analysis showed oligoasthenospermia. He denied using exogenous testosterone. Scrotal ultrasound showed microlithiasis and millimetric hypolucent lesions in the left testis but no intratesticular mass. Human chorionic gonadotropin was low. To investigate unilateral hormone secretion, selective testicular venous sampling was performed. Testosterone and estradiol were clearly higher on the left side than on the right (130 vs 26 nmol/L and 1388 vs 62 pmol/L, respectively), with a left spermatic vein–to-periphery gradient of 4.3 for testosterone and 13 for estradiol; there were no similar gradients on the right side. This finding confirms that all sex steroid secretion came from the left testis. The patient was therefore referred for left orchidectomy. Histopathology revealed multifocal seminoma, germ cell neoplasia in situ, and Leydig cell hyperplasia but no choriocarcinoma. However, gonadotrophin levels increased after orchidectomy, indicating that the source of gonadotropin-independent sex steroid secretion was removed. Testosterone and estradiol decreased to the mid-normal range. Sperm concentration improved. This report thus shows that endogenous testosterone secretion in one testicle supports spermatogenesis without measurable levels of gonadotropins. Selective testicular venous sampling is useful to identify the site of unilateral secretion when the clinical picture is inconclusive. However, histopathology could not reveal the factor that stimulated Leydig cell steroidogenesis.

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Dissertations / Theses on the topic "Gonadotrophin secretion"

1

Honaramooz, Ali. "Neuroendocrinology of gonadotrophin secretion in prepubertal heifers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ37889.pdf.

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Durnin, Anne Theresa. "Secretory heterogeneity among anterior pituitary gonadotrophs." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358632.

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Wood, Sara C. "Ovarian regulation of pituitary gonadotrophin secretion in domestic ruminants." Thesis, University of Reading, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333527.

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Buckler, Helen Margaret. "Gonadotrophin, inhibin and sex steroid secretion in disorders of ovulation." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305188.

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Dodson, S. E. "Reproductive endocrinology of the heifer from birth to the peripubertal period." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376401.

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Lewis, C. E. "Factors involved in control of gonadotrophin secretion by the anterior pituitary gland." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375271.

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Forsdike, Rachel Anne. "In utero development of sexually dimorphic gonadotrophin-releasing hormone (GnRH) secretion in sheep." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620917.

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Castillo, R. J. "Bioassay and isolation of bovine ovarian inhibin and its effects on gonadotrophin secretion." Thesis, University of Reading, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233158.

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9

Evans, Neil Price. "The regulation of gonadotrophin secretion following divergent selection for pituitary responsiveness to GnRH." Thesis, University of Edinburgh, 1991. http://hdl.handle.net/1842/19730.

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Divergent selection based on the LH response to a 5μg dose of GnRH, has created two lines of sheep which differ in their ability to release gonadotrophins in response to a GnRH challenge in both male and female lambs. Significant correlated between line differences have also been reported in female reproductive performance. The aim of this project was to investigate the regulation of gonadotrophin secretion in animals from the two lines, and to elucidate the primary site of the selected difference/s. Physiological studies of adult ewes and prepubertal ram lambs demonstrated that despite similar peripheral steroid concentrations, endogenous and exogenously stimulated gonadotrophin secretion differed significantly between the two lines. Mean LH and FSH concentrations in the prepubertal male lambs were significantly higher in the High line than the Low line, due to the secretion of LH pulses of significantly greater amplitude by the High line ram lambs. Similarly, higher amplitude LH pulses were observed in the High line ewes during the follicular phase of the oestrous cycle. The age related changes in basal LH secretion in the ram lambs and the observation of significant differences in LH pulse amplitude in the adult ewes during the follicular phase of the oestrous cycle, when progesterone negative feedback is reduced, indicate that the effects of the between line difference in the regulation of endogenous LH secretion are regulated by gonadal negative feedback. However studies in prepubertal ram lambs demonstrated that the primary site of the selected difference was at the level of the hypothalamo/pituitary gland complex. Studies of the regulation of LH secretion by the hypothalamo/pituitary gland complex demonstrated that the High line lambs appeared to secrete significantly less GnRH than the Low line and that the pituitary glands of the High line were 5 fold more sensitive to GnRH than the Low line. Pituitary sensitivity encompasses a large number of variables, including gonadotrophe and GnRH receptor number, the intracellular events which follow receptor activation and the amount of releasable LH stored in the pituitary gland, the individual or combined effects of which could result in differences in pituitary sensitivity. Pituitary gonadotrophe number/size was studied indirectly as a function of pituitary gland weight. The pituitary glands obtained from the High line tended to be heavier than those obtained from the Low line, however this difference was not statistically significant. The pituitary glands of the High line were also found to contain significantly more GnRH receptors/mg of protein than the Low line. The importance of this difference with regard to pituitary sensitivity was questioned, however, following the demonstration that the between line difference in the magnitude of the LH response was maintained in vitro following either GnRH stimulated LH release or the direct stimulation of both the Ca^2+-calmodulin and Protein Kinase C second messenger systems. Examination of the pituitary stores of LH in the two lines demonstrated that the 5μg dose of GnRH used in the selection programme stimulated a maximal release of LH in both lines, and that the High line stored significantly greater quantities of releasable LH compared with the Low line. The results also indicated that the two lines may differ in their ability to synthesise LH in response to GnRH stimulation.

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Lujan, Marla Elaine. "The effects of stimulating endogenous corticotrophin-releasing hormone on gonadotrophin secretion in rhesus monkeys." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63331.pdf.

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Books on the topic "Gonadotrophin secretion"

1

Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Leeuw, Renato de. Regulation of gonadotropin secretion in the African catfish, Clarias gariepinus (Burchell) =: Regulatie van de gonadotroop hormoon Afgifte in de Afrikaanse meerval, Clarias gariepinus (Burchell). Utrecht: Drukkerij Elikwijk BV, 1985.

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Bower, Mark, Louise Robinson, and Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.

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Cancer produces endocrine and metabolic complications in two ways. Firstly, the primary tumour or its metastases may interfere with the function of endocrine glands, kidneys, or liver by invasion or obstruction. Secondly, tumours may give rise to remote effects without local spread and these actions are termed paraneoplastic manifestations of malignancy. Generally, these paraneoplastic syndromes arise from secretion by tumours of hormones, cytokines, and growth factors, but also occur when normal cells secrete products in response to the presence of tumour. This chapter reviews the pathogenesis, epidemiology, and management of the commonest paraneoplastic endocrinopathies including hypercalcaemia, Cushing’s syndrome, the syndrome of inappropriate antidiuresis, non-islet cell tumour hypoglycaemia, enteropancreatic hormone syndromes, Carcinoid syndrome, phaeochromocytoma, gonadotrophin secretion syndromes, prolactin and oxytocin secretion, and paraneoplastic pyrexia. The chapter concludes with a brief discussion of the management of metabolic disease in the context of advanced malignancy including hyperglycaemia, thyroid dysfunction, metabolic bone disease, renal failure, liver failure, and lactic acidosis.

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Butler, Gary, and Jeremy Kirk. Puberty and its disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0018.

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Definition 44Physiology of normal puberty 46Pubertal staging 48Timing of puberty 52Premature sexual maturation 53Central precocious puberty (CPP) (gonadotropin-dependent precocious puberty) 54Abnormal patterns of gonadotropin secretion 56Gonadotropin-independent precocious puberty (GIPP) 57Virilization 58Delayed puberty 60Central causes of delayed puberty (both sexes) ...

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Butler, Gary, and Jeremy Kirk. Endocrine investigations and laboratory reference ranges. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0101.

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General guidelines 330GH provocation tests 331Tests for GH secretion 332IGF-1 generation test 334Oral glucose tolerance test for investigating excess GH secretion 335TRH test 336LHRH/GnRH (gonadotropin-releasing hormone) stimulation test 337Triple pituitary stimulation test 338Water deprivation test (WDT) 340...

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Jaeger, John Ralph. Gonadotropin releasing hormone-induced secretion of luteinizing hormone during the milk ejection reflex in the postpartum beef cow. 1986.

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B, Mahesh Virendra, ed. Regulation of ovarian and testicular function. New York: Plenum Press, 1987.

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R, Rolland, Chadha Dev R, and Willemsen, Wilhelmus Nicolass Petrus, 1947-, eds. Gonadotropin down-regulation in gynecological practice: Proceedings of an international symposium held at the University of Nijmegen, the Netherlands, April 25 and 26, 1986. New York: Liss, 1986.

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Book chapters on the topic "Gonadotrophin secretion"

1

Lincoln, Gerald. "Melatonin Modulation of Prolactin and Gonadotrophin Secretion." In Advances in Experimental Medicine and Biology, 137–53. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46814-x_16.

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Banks, P. J., H. M. Lloyd, and E. F. Scowen. "Gonadotrophin Excretion in Man." In Ciba Foundation Symposium - Anterior Pituitary Secretion (Book I of Colloquia on Endocrinology, Vol. 4), 283–93. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718803.ch26.

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Dawson, Alistair. "Photoperiodic Control of Gonadotrophin-Releasing Hormone Secretion in Seasonally Breeding Birds." In Neural Regulation in the Vertebrate Endocrine System, 141–59. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4805-8_10.

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Götz, Franziska, Wolfgang Rohde, and Günter Dörner. "Neuroendocrine Differentiation of Sex-Specific Gonadotrophin Secretion, Sexual Orientation and Gender Role Behaviour." In Heterotypical Behaviour in Man and Animals, 167–94. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3078-3_7.

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Crooke, A. C. "The Influence of Certain Adrenergic and Cholinergic Drugs on Urinary Gonadotrophin output in Amenorrhœic Women." In Ciba Foundation Symposium - Anterior Pituitary Secretion (Book I of Colloquia on Endocrinology, Vol. 4), 179–85. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718803.ch16.

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Genazzani, A. R., F. Petraglia, S. Angioni, G. Comitini, S. Bettelli, B. Preti, F. Amato, N. Tesorio, and M. C. Galassi. "Opioid Control of Gonadotropin Secretion." In Endorphins in Reproduction and Stress, 3–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75797-6_1.

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Burger, H. G. "Regulation of Gonadotropin Secretion: A 1987 Perspective." In Neuroendocrine Perspectives, 107–17. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3478-4_13.

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Everett, John W. "Timing the Preovulatory Surge of Gonadotropin Secretion." In Neurobiology of Reproduction in the Female Rat, 38–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83797-5_6.

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Flerkó, Béla, István Merchenthaler, and György Sétáló. "Short and Ultrashort Feedback Control of Gonadotropin Secretion." In Endocrinology and Physiology of Reproduction, 37–50. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-1971-7_5.

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Leyendecker, G., and L. Wildt. "Hypothalamic control of gonadotropin secretion and ovarian function." In LH-RH and its Analogues, edited by Manfred Schmidt-Gollwitzer and Rosemarie Schley, 13–24. Berlin, Boston: De Gruyter, 1985. http://dx.doi.org/10.1515/9783110861488-004.

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