Journal articles: 'Gonadotropin-Releasing hormones'

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Podhorec, P., and J. Kouril. "Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review." Veterinární Medicína 54, No. 3 (April 8, 2009): 97–110. http://dx.doi.org/10.17221/50/2009-vetmed.

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Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.

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Saleh, Ahmed A., Nada N. A. M. Hassanine, Taha K. Taha, Amr M. A. Rashad, and Mahmoud A. Sharaby. "Molecular regulation and genetic basis of gonadotropin-releasing hormone genes: A review." Applied Veterinary Research 2, no. 4 (October 10, 2023): 2023017. http://dx.doi.org/10.31893/avr.2023017.

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This review systematically introduces basic information on the hypothalamic pituitary-gonad axis and provides knowledge on the regulation, location, function, reproduction, gene mutations, disorders, sexual behavior, life cycle, and effect of environmental factors on the gonadotropin-releasing hormone gene. On the other hand, this review focused on the GnRH gene, regulations, receptor structures, and their signaling pathways, in addition to its related genes and its effect on crucial hormones such as follicle-stimulating hormone, luteinizing hormone, testosterone, estradiol, and progesterone. Additionally, gonadotropin-inhibiting hormone and its related peptides, such as R-Famide peptides, were found to decrease hormone secretion by working on the hypothalamic pituitary gonads axis to inhibit the biosynthesis process of gonadotropin alpha and beta subunits. Additionally, the roles of crucial hormones in reproduction and fertility, as well as the disruption, resulted from mutations. Special characteristics of several hormones and pulsatile secretion of gonadotropin-releasing hormone were also summarized.

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Crowley, W. R. "Toward Multifactorial Hypothalamic Regulation of Anterior Pituitary Hormone Secretion." Physiology 14, no. 2 (April 1999): 54–58. http://dx.doi.org/10.1152/physiologyonline.1999.14.2.54.

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The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.

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King, Judy A., and Robert P. Millar. "Evolution of gonadotropin-releasing hormones." Trends in Endocrinology & Metabolism 3, no. 9 (November 1992): 339–46. http://dx.doi.org/10.1016/1043-2760(92)90113-f.

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SHERWOOD, NANCY M., DAVID A. LOVEJOY, and IMOGEN R. COE. "Origin of Mammalian Gonadotropin-Releasing Hormones." Endocrine Reviews 14, no. 2 (April 1993): 241–54. http://dx.doi.org/10.1210/edrv-14-2-241.

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Pehlivan, Erkan, Hüseyin Polat, and Gürsel Dellal. "Annual Change of Reproductive Hormones in Female Angora Goats." Turkish Journal of Agriculture - Food Science and Technology 5, no. 4 (April 6, 2017): 343. http://dx.doi.org/10.24925/turjaf.v5i4.343-348.1220.

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In this research, annual changes of melatonin, gonadotropin-releasing hormone, follicle stimulating hormone, luteinizing hormone, estrogen, testosterone and progesterone were studied on 6 heads of 1.5 years old female Angora goat. To determine hormones concentrations, blood samples were taken from jugular vein of each goat in every month for a year. The blood samples were centrifuged at 4000xg for 5 min. and serum was stored at -20°C until analyses time. Hormones analyses in the serum were performed by enzyme immunoassay (EIA) method. Monthly climatic values and photoperiod were obtained from the Turkish State Meteorological Service and temperature-humidity index was calculated with climatic values. In the study, in order to determine any possible differences in the observed hormones concentrations with respect to months, repeated measures ANOVA analysis was performed. As a result of statistical analysis, there were no significant differences among the months for gonadotropin-releasing hormone, follicle stimulating hormone and testosterone concentration, while significant differences were found among the months for melatonin, luteinizing hormone and progesterone, and estrogen concentration in female Angora goats. According the results of this study, could be concluded that the releases of reproductive hormones examined in female Angora goats was seasonally dependent.

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Kotlyar, Alexander M., Lubna Pal, and Hugh S. Taylor. "Eliminating Hormones With Orally Active Gonadotropin-releasing Hormone Antagonists." Clinical Obstetrics & Gynecology 64, no. 4 (October 21, 2021): 837–49. http://dx.doi.org/10.1097/grf.0000000000000664.

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Richalet, Jean-Paul, Murielle Letournel, and Jean-Claude Souberbielle. "Effects of high-altitude hypoxia on the hormonal response to hypothalamic factors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 6 (December 2010): R1685—R1692. http://dx.doi.org/10.1152/ajpregu.00484.2010.

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Acute and chronic exposure to high altitude induces various physiological changes, including activation or inhibition of various hormonal systems. In response to activation processes, a desensitization of several pathways has been described, especially in the adrenergic system. In the present study, we aimed to assess whether the hypophyseal hormones are also subjected to a hypoxia-induced decrease in their response to hypothalamic factors. Basal levels of hormones and the responses of TSH, thyroid hormones, prolactin, sex hormones, and growth hormone to the injection of TRH, gonadotropin-releasing hormone, and growth hormone-releasing hormone (GHRH) were studied in eight men in normoxia and on prolonged exposure (3–4 days) to an altitude of 4,350 m. Thyroid hormones were elevated at altitude (+16 to +21%), while TSH levels were unchanged, and follicle-stimulating hormone and prolactin decreased, while leutinizing hormone was unchanged. Norepinephrine and cortisol levels were elevated, while no change was observed in levels of epinephrine, dopamine, growth hormone (GH), IGF-1, and IGFBP-3. The mean response to hypothalamic factors was similar in both altitudes for all studied hormones, although total T4 was lower in hypoxia during 45 to 60 min after injection. The effect of hypoxia on the hypophyseal response to hypothalamic factors was similar among subjects, except for the GH response to GHRH administration. We conclude that prolonged exposure to high-altitude hypoxia induces contrasted changes in hormonal levels, but the hypophyseal response to hypothalamic factors does not appear to be blunted.

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Muñoz-Cueto, José A., Nilli Zmora, José A. Paullada-Salmerón, Miranda Marvel, Evaristo Mañanos, and Yonathan Zohar. "The gonadotropin-releasing hormones: Lessons from fish." General and Comparative Endocrinology 291 (May 2020): 113422. http://dx.doi.org/10.1016/j.ygcen.2020.113422.

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Chen, Huiqin, Baoliang Bi, Lingfu Kong, Hua Rong, Yanhua Su, and Qing Hu. "Seasonal Changes in Plasma Hormones, Sex-Related Genes Transcription in Brain, Liver and Ovary during Gonadal Development in Female Rainbow Trout (Oncorhynchus mykiss)." Fishes 6, no. 4 (November 12, 2021): 62. http://dx.doi.org/10.3390/fishes6040062.

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The purpose of this study was to investigate the periodic seasonal changes in endocrine activity and gonadal development of female rainbow trout (Oncorhynchus mykiss) in a high-altitude cold-water environment. The fish were sampled monthly from January to November and the levels of plasma hormones (estradiol (E2), cortisol and thyroid hormones (THS)) and vitellogenin (VTG) were measured by ELISA. Moreover, the transcriptions of sex-related genes in the ovary, brain, and liver were detected by qRT-PCR. The results showed a seasonal fluctuation of plasma hormones and VTG together with the development of the ovary, which reached a peak from August to October. Similarly, the transcription of hypothalamic gonadotropin-releasing hormone-2 (cgnrh-2), hypothalamic gonadotropin-releasing hormone receptors (gnrhr) and follicle-stimulating hormone (fsh) in the brain varied from January to September, but the highest level was detected in September to November. In addition, the transcription of sex-related genes located in the ovary and liver increased significantly during August to October, accompanied by a continuous increase in the gonadosomatic index (GSI) and a decrease in the hepatosomatic index (HSI). Therefore, plasma hormones and sex-related genes regulate the development and maturation of O. mykiss oocytes with the change in seasons and peaked in November. The results of this study provide a reference for improving the efficiency of the artificial reproduction of O. mykiss.

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Sahadan, Fatin Nabilah, Annie Christianus, Ina-Salwany Md Yasin, Fadhil-Syukri Ismail, Roshani Othman, and Zarirah Zulperi. "Gonadotropin-Releasing Hormone (GnRH)- Its Approaches to Improve Reproduction in Fish." Sains Malaysiana 51, no. 11 (November 30, 2021): 3539–49. http://dx.doi.org/10.17576/jsm-2022-5111-03.

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This review briefly highlights previous studies on the gonadotropin-releasing hormone (GnRH) and its approaches to improving fish reproduction in the aquaculture industry. Reproductive system dysfunction of the captive fish is the main problem that has to be treated depending on the compatibility of fish species. This problem is caused by the non-synchronized maturation of female and male broodstock, and the low quality of broodstock. As shown in previous studies, induced breeding with exogenous treatment from specialized hormones could be one of the best cures for this issue. Hormonal treatments have been used by farmers to overcome the reproductive system dysfunctions in establishing captive wild or hatchery-based breeding. Although the imitation in its natural condition has been set up, for broodstock to spawn naturally problems still occur, hence the need for hormonal therapy. This review aims to deliver the results and contributions of an established artificial hormone, gonadotropin-releasing hormone analogue (GnRHa), to treat fish reproductive system dysfunction, to improve the qualities of eggs, seedlings, and broodstock, mainly to help fish farmers and can be used in the aquaculture industry to improve the reproduction of cultured fishes for sustainable aquaculture production to achieve the market demand and consumption.

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Zheng, H., J. J. Kavanagh, W. Hu, Q. Liao, and S. Fu. "Hormonal therapy in ovarian cancer." International Journal of Gynecologic Cancer 17, no. 2 (2007): 325–38. http://dx.doi.org/10.1111/j.1525-1438.2006.00749.x.

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Ovarian carcinoma continues to be the leading cause of death due to gynecological malignancy. Epidemiologic studies indicate that steroid hormones play roles in ovarian carcinogenesis. Gonadotropins, estrogen, and androgen may be causative factors, while gonadotropin-releasing hormone and progesterone may be protective factors in ovarian cancer pathogenesis. Experimental studies have shown that hormonal receptors are expressed in ovarian cancer cells and mediate the growth-stimulatory or growth-inhibitory effects of the hormones on these cells. Hormonal therapeutic agents have been evaluated in several clinical trials. Most of these trials were conducted in patients with recurrent or refractory ovarian cancer, with modest efficacy and few side effects. Better understanding of the mechanisms through which hormones affect cell growth may improve the efficacy of hormonal therapy. Molecular markers that can reliably predict major clinical outcomes should be investigated further in well-designed trials

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Collins, Taylor, and Krista L. Rompolski. "Hypothalamic Amenorrhea: Causes, Complications, & Controversies." Journal of Student Research 6, no. 1 (May 23, 2017): 24–32. http://dx.doi.org/10.47611/jsr.v6i1.288.

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Hypothalamic amenorrhea (HA) is considered a reversible condition characterized by the absence of menses for 3 months or more, due to suppressed secretions of gonadotropin releasing hormone affecting the entire hypothalamic-pituitary-ovarian axis. HA can be triggered by excessive stress, weight loss or excessive exercise, however, the etiology is still largely unknown. Serious, long-term complications include severe hypoestrogenism and infertility, in addition to a variety of hormonal aberrations. Hypoestrogenism also leads to diminished bone health, cardiovascular problems, and mood changes that lead to a higher prevalence of depression and anxiety. It is important that HA is diagnosed in a timely manner in order to begin therapeutic strategies that aim to resume menses and return to normal levels of circulating reproductive hormones. When attempts to resume menstruation naturally through lifestyle changes are unsuccessful, other pharmaceutical options are available. Treatment options range from estrogen-replacement therapy to the administration of gonadotropin releasing hormone, depending on the reproductive goals of the woman. More research is needed on novel treatments in order to determine the most effective standard of care.

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Schiml, Patricia A., and Emilie F. Rissman. "Effects of Gonadotropin-Releasing Hormones, Corticotropin-Releasing Hormone, and Vasopressin on Female Sexual Behavior." Hormones and Behavior 37, no. 3 (May 2000): 212–20. http://dx.doi.org/10.1006/hbeh.2000.1575.

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Bourne, G. A., and D. M. Baldwin. "Evidence for cAMP as a mediator of gonadotropin secretion from male pituitaries." American Journal of Physiology-Endocrinology and Metabolism 253, no. 3 (September 1, 1987): E296—E299. http://dx.doi.org/10.1152/ajpendo.1987.253.3.e296.

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The purpose of this study was to use sodium flufenamate, a compound that inhibits gonadotropin-releasing hormone (GnRH)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in the pituitary, to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion from male pituitaries. Quartered male pituitaries were perifused at 37 degrees C and sequential effluent fractions collected every 10 min. Infusions of GnRH resulted in a twofold increase in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Cycloheximide, 5 microM, completely inhibited the GnRH-stimulated LH and FSH secretion. Infusions of 0.1 mM flufenamate had similar effects on gonadotropin secretion as cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate restored the secretory responses of both hormones. The flufenamate-inhibited GnRH stimulated LH and FSH release, which was restored by DBcAMP and appeared to be protein synthesis dependent and specific for cAMP. These results suggest an indirect role for cAMP as a mediator of gonadotropin secretion from male pituitaries. However, in contrast to female pituitaries, the secretion of these hormones from male pituitaries is completely dependent on cAMP and de novo protein synthesis.

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GOOS, HENK J. TH, MARION BLOMENROHR, JAN BOGERD, PETER T. BOSMA, KA W. LI, KOICHI OKUZAWA, FRANK E. M. REBERS, RUDIGER W. SCHULZ, CEES P. TENSEN, and MATTHYS A. ZANDBERGEN. "Gonadotropin-Releasing Hormones and Their Receptors in Fish." Annals of the New York Academy of Sciences 839, no. 1 TRENDS IN COM (May 1998): 41–46. http://dx.doi.org/10.1111/j.1749-6632.1998.tb10730.x.

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Sharp, Peter J., and Dominique Blache. "A neuroendocrine model for prolactin as the key mediator of seasonal breeding in birds under long- and short-day photoperiods." Canadian Journal of Physiology and Pharmacology 81, no. 4 (April 1, 2003): 350–58. http://dx.doi.org/10.1139/y03-025.

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Seasonal breeding is associated with sequential increases in plasma luteinizing hormone (LH) and prolactin in the short-day breeding emu, and in long-day breeding birds that terminate breeding by the development of reproductive photorefractoriness. A model of the avian neuroendocrine photoperiodic reproductive response is proposed, incorporating a role for prolactin, to account for neuroendocrine mechanisms controlling both long- and short-day breeding. The breeding season terminates after circulating concentrations of prolactin increase above a critical threshold to depress gonadotropin releasing hormone (GnRH) neuronal and gonadotrope (LH) activity. Subsequently, photorefractoriness develops for prolactin secretion and for LH secretion, independently of high plasma prolactin. The breeding season in the emu is advanced compared with long-day breeders, because after photorefractiness for both LH and prolactin secretion is dissipated, plasma concentrations of both hormones increase to maximum values while days are still short.Key words: seasonal breeding, prolactin, gonadotropin releasing hormone, photorefactoriness.

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Toth, Michael J., Brian C. Cooper, Richard E. Pratley, Andrea Mari, Dwight E. Matthews, and Peter R. Casson. "Effect of ovarian suppression with gonadotropin-releasing hormone agonist on glucose disposal and insulin secretion." American Journal of Physiology-Endocrinology and Metabolism 294, no. 6 (June 2008): E1035—E1045. http://dx.doi.org/10.1152/ajpendo.00789.2007.

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Several lines of evidence suggest that ovarian hormones influence glucose homeostasis, although their exact role in humans has not been clearly defined. In the present study, we sought to test the hypothesis that ovarian hormones regulate glucose homeostasis by examining the effect of pharmacologically induced ovarian hormone deficiency on glucose disposal and insulin secretion. Young, healthy women with regular menstrual patterns were studied during the follicular and luteal phases of their cycle at baseline and after 2 mo of treatment with gonadotropin-releasing hormone agonist (GnRHa; n = 7) or placebo ( n = 6). Using hyperglycemic clamps, in combination with stable isotope-labeled (i.e., 13C and 2H) glucose tracers, we measured glucose disposal and insulin secretion. Additionally, we assessed body composition and regional fat distribution using radiologic imaging techniques as well as glucoregulatory hormones. Ovarian hormone suppression with GnRHa did not alter body composition, abdominal fat distribution, or thigh tissue composition. There was no effect of ovarian suppression on total, oxidative, or nonoxidative glucose disposal expressed relative to plasma insulin level. Similarly, no effect of ovarian hormone deficiency was observed on first- or second-phase insulin secretion or insulin clearance. Finally, ovarian hormone deficiency was associated with an increase in circulating adiponectin levels but no change in leptin concentration. Our findings suggest that a brief period of ovarian hormone deficiency in young, healthy, eugonadal women does not alter glucose disposal index or insulin secretion, supporting the conclusion that ovarian hormones play a minimal role in regulating glucose homeostasis. Our data do, however, support a role for ovarian hormones in the regulation of plasma adiponectin levels.

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Yilmaz, Nafiye, Necati Hancerliogullari, Mustafa Kara, and Yaprak Engin-Ustun. "Is gonadotropin-releasing hormone agonist usage really leading to thyroid dysfunction?" Interventional Medicine and Applied Science 11, no. 3 (September 16, 2020): 136–38. http://dx.doi.org/10.1556/1646.10.2018.32.

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Objectives Gonadotropin-releasing hormone agonist (GnRHa) could influence the levels of sex hormones and thyroid hormones. The aim of this study was to investigate the effect of GnRHa on thyroid function. Materials and methods The data of the patients were collected from the registrations of July 2014–October 2014. A total of 41 women who underwent one-time IVF cyclus were evaluated in this cross-sectional study. The patients were categorized into two groups according to the serum T3, T4, and TSH levels before and 2 weeks’ after the administration of GnRHa. Results Mean basal TSH and mean TSH levels on hCG day were 1.98 ± 0.77 and 1.75 ± 0.70, respectively. The difference between the two groups was statistically significant (p < 0.05). GnRHa did not lead to statistically significant difference on serum-free T3 and T4 levels. Conclusions In conclusion, our results demonstrate that GnRHa led to a decrease on serum TSH level. Serum-free T3 and T4 levels were remained unchanged and this might be due to early measurement of the hormone levels (just 2 weeks later from GnRHa administration).

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Malakheeva, Lidiya, Alexey Komarchev, Yegor Kulikov, and Lyudmila Korshunova. "Gonadotropin concentration changing dynamics in producing layers during ovulatory cycle." Poultry and Chicken Products 25, no. 4 (2023): 36–39. http://dx.doi.org/10.30975/2073-4999-2023-25-4-36-39.

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The paper has been devoted to study of gonadotropic hormone content dynamics in layer blood during ovu- latory cycle for it reference meanings range definition and determining of physiologic and endocrine mechanisms inter- relations that influence on ovulatory cycle. Total calcium level in layer blood has been given that is necessary for positive feedback creation between progesterone and impulse release of gonadotropin-releasing hormones (GRH). Follicle-stim- ulating and luteinizing hormones content in layer blood plasma and serum have been determined by solid phase immune enzymatic analysis and calcium content has been determined by biochemical method with flowing semi-automatic bio- chemical analyzer. Optimization of definition method has been suggested for hormone levels.

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Bonnin, M., M. Mondain-Monval, M. C. Audy, and R. Scholler. "Basal and gonadotropin releasing hormone stimulated gonadotropin levels in the female red fox (Vulpes vulpes L.). Negative feedback of ovarian hormones during anoestrus." Canadian Journal of Zoology 67, no. 3 (March 1, 1989): 759–65. http://dx.doi.org/10.1139/z89-107.

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In the red fox, Vulpes vulpes L., an inhibition of gonadotropic function is observed in early anoestrus, particularly during lactation. During this period, secretion of progesterone as a result of the persistent corpora lutea after parturition and episodic releases of estradiol signify ovarian activity, suggesting involvement of these hormones in the modulation of pituitary hormones (luteinizing hormone (LH), follicle-stimulating hormone (FSH)). Effects of ovariectomy and (or) progesterone or estradiol treatments in vivo upon basal and gonadotropin releasing hormone (GnRH)-stimulated LH and FSH were observed. After ovariectomy, a great increase in the basal level of both gonadotropins and in GnRH-stimulated LH release, but not GnRH-stimulated FSH release, were observed. Progesterone treatment induced a decrease in GnRH-stimulated LH and FSH secretions and a decrease in basal LH and FSH levels in ovariectomized females. Estradiol treatment abolished basal secretions and GnRH responses for both hormones. These results suggest a negative feedback of both ovarian steroids at the hypothalamopituitary level on LH and FSH secretions during early anoestrus.

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Ukrainets, Roman V., and Yulia S. Korneva. "Endometrial cell apoptosis impairment associated with hormonal imbalance as a key factor in the development of endometriosis." Problems of Endocrinology 65, no. 2 (June 30, 2019): 140–44. http://dx.doi.org/10.14341/probl9983.

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The review describes the effect of certain hormones and their imbalance on apoptosis of retrogradely refluxed endometrial cells in the abdominal cavity and the effects of estrogen, progesterone, anti-Mullerian hormone, and gonadotropin-releasing hormone on the internal and external apoptotic pathways of various cell populations in endometriotic foci. The nuclear estrogen receptor (ER-) is shown to inhibit TNF receptors that trigger the external apoptotic pathway, but the effects of estrogens do not play a key role in the pathogenesis of endometriosis. The role of progesterone and changes in the receptor status towards prevalence of PR-A with a decreased response of endometrial tissue to progesterone and inhibition of apoptosis are described. We discuss the role of the anti-Mllerian hormone and gonadotropin-releasing hormone II (GnRH II) as activators of apoptosis in normal endometrial tissue and in endometriosis. Investigation of endocrine effects on apoptosis of parenchymal and stromal cells of endometriotic foci may provide a theoretical basis for searching for new therapeutic targets in this hormone-dependent pathology.

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Bourne, G. A., and D. M. Baldwin. "Evidence for cAMP as a mediator of gonadotropin secretion from female pituitaries." American Journal of Physiology-Endocrinology and Metabolism 253, no. 3 (September 1, 1987): E290—E295. http://dx.doi.org/10.1152/ajpendo.1987.253.3.e290.

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Sodium flufenamate, which inhibited gonadotropin-releasing hormone (GnRH)-stimulated increases in adenosine 3',5'-cyclic monophosphate (cAMP), was used to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion. Quartered pituitaries from diestrous II female rats were perifused at 37 degrees C, and sequential effluent fractions were collected every 10 min. Administration of GnRH resulted in a characteristic biphasic response for both luteinizing hormone (LH) and follicle-stimulating hormone (FSH), whereas 5 microM cycloheximide inhibited the secondary augmented responses (phase II) of both hormones. Infusions of 0.1 mM flufenamate inhibited GnRH-stimulated gonadotropin secretion in a manner similar to that of cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate resulted in the restoration of LH and FSH secretion. The dibutyryl cAMP-restored response appeared to be protein synthesis dependent and specific for cAMP. These results suggest that although the cyclic nucleotide is not involved in the acute release of LH and FSH, it does appear to play a pivotal but indirect role in phase II release of the hormones, by effects involving the stimulation of de novo protein synthesis.

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Bédécarrats, Grégoy Y., Mamiko Shimizu, and Daniel Guémené. "Gonadotropin Releasing Hormones and their Receptors in Avian Species." Journal of Poultry Science 43, no. 3 (2006): 199–214. http://dx.doi.org/10.2141/jpsa.43.199.

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PETER, R. E., H. R. HABIBI, T. A. MARCHANT, and C. S. NAHORNIAK. "Vertebrate Gonadotropin-Releasing Hormones: Phylogeny and Structure-Function Relationships." Annals of the New York Academy of Sciences 519, no. 1 The Terminal (December 1987): 299–309. http://dx.doi.org/10.1111/j.1749-6632.1987.tb36305.x.

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Moghissi, Kamran S. "Clinical Applications of Gonadotropin-Releasing Hormones in Reproductive Disorders." Endocrinology and Metabolism Clinics of North America 21, no. 1 (March 1992): 125–40. http://dx.doi.org/10.1016/s0889-8529(18)30235-4.

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Bogerd, Jan, Ka Wan Li, Coby Janssen-Dommerholt, and Henk Goos. "Two gonadotropin-releasing hormones from African catfish (Clarias gariepinus)." Biochemical and Biophysical Research Communications 187, no. 1 (August 1992): 127–34. http://dx.doi.org/10.1016/s0006-291x(05)81468-8.

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Peter, R. E., C. S. Nahorniak, S. Shih, J. A. King, and R. P. Millar. "Activity of position-8-substituted analogs of mammalian gonadotropin-releasing hormone (mGnRH) and chicken and lamprey gonadotropin-releasing hormones in goldfish." General and Comparative Endocrinology 65, no. 3 (March 1987): 385–93. http://dx.doi.org/10.1016/0016-6480(87)90123-7.

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Tena-Sempere, Manuel, and Ilpo Huhtaniemi. "Sex in the brain: How the brain regulates reproductive function." Biochemist 31, no. 2 (April 1, 2009): 4–7. http://dx.doi.org/10.1042/bio03102004.

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Reproductive functions are maintained by a complex hormonal regulatory network called the hypothalamic–pituitary–gonadal (HPG) axis, which is under the hierarchical control of a network of neurohormones that ultimately modulate the synthesis and pulsatile release of the decapeptide gonadotropin-releasing hormone (GnRH) by specialized neural cells distributed along the mediobasal hypothalamus. This neuropeptide drives the production of the two gonadotropic hormones of the anterior pituitary gland, luteinizing hormone (LH) and folliclestimulating hormone (FSH), which are released into the circulation and regulate specific functions of the ovary and testis. In turn, hormones produced by the gonads feed back to the hypothalamic– pituitary level to maintain functional balance of the HPG axis, through negative and positive (only in females) regulatory loops. In this article, we review the main hormonal regulatory systems that are operative in the HPG axis with special emphasis on recent developments in our knowledge of the neuroendocrine pathways governing GnRH secretion, including the identification of kisspeptins and G-protein-coupled receptor 54 (GPR54) as major gatekeepers of puberty onset and fertility.

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Kraak, G. Van Der, E. M. Donaldson, H. M. Dye, G. A. Hunter, J. E. Rivier, and W. W. Vale. "Effects of Mammalian and Salmon Gonadotropin-Releaslng Hormones and Analogues on Plasma Gonadotropin Levels and Ovulation in Coho Salmon (Oncorhynchus kisutch)." Canadian Journal of Fisheries and Aquatic Sciences 44, no. 11 (November 1, 1987): 1930–35. http://dx.doi.org/10.1139/f87-237.

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The effects of intraperitoneal injections of mammalian gonadotropin-releasing hormone (mGnRH) and salmon gonadotropin-releasing hormone (sGnRH; [Trp7, Leu8]-mGnRH) as well as analogues of each peptide on plasma gonadotropin levels and ovulation in coho salmon (Oncorhynchus kisutch) were investigated. The native peptides had similar potencies in terms of the magnitude and duration of the gonadotropin release response. Analogues including the D-Ala6 and (imbz1) D-His6 derivatives of [Pro9-NEt]-mGnRH and the D-Arg6 and D-Ala6 derivatives of [Pro9-NEt]-sGnRH stimulate a more prolonged increase in plasma gonadotropin levels than native forms of these peptides. Each of the analogue peptides at a dosage of 0.2 mg/kg body wt induced a high rate of ovulation; the native salmon peptide at the same dosage was also effective although the time of ovulation was delayed compared with the response to analogue peptides. A higher dosage of the native salmon peptide (1.0 mg/kg body wt) was less effective in stimulating gonadotropin release and failed to induce a high rate of ovulation. Our studies demonstrate that several analogues of mGnRH and sGnRH have superactive agonist activity in coho salmon and are effective in inducing ovulation in this species.

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Bain, J., R. Langevin, S. Hucker, R. Dickey, P. Wright, and C. Schonberg. "Sex Hormones in Pedophiles: I Baseline Values of Six Hormones Ii the Gonadotropin Releasing Hormone Test." Sexual Abuse: A Journal of Research and Treatment 1, no. 3 (January 1, 1988): 443–54. http://dx.doi.org/10.1177/107906328800100306.

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Shukla, Akshara, Rohitash Jamwal, and Kumud Bala. "ADVERSE EFFECT OF COMBINED ORAL CONTRACEPTIVE PILLS." Asian Journal of Pharmaceutical and Clinical Research 10, no. 1 (January 1, 2016): 17. http://dx.doi.org/10.22159/ajpcr.2017.v10i1.14565.

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ABSTRACTOral contraceptive (OC) pills contain estrogen and progestin that are synthetic analogs of natural hormones. These synthetic hormones affectthe hypothalamus-pituitary-gonadal axis of the female reproductive system. There are many types of contraceptives; most of the OC pills preventpregnancy by inhibiting ovulation. Estrogen and progestin are two female reproductive hormones that are critical. Typically, estradiol is producedby growing follicle (ovaries) which stimulates the hypothalamus to produce the gonadotropin-releasing hormone, which further stimulates theanterior pituitary to produce follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH production triggers the ovulation. Similarly, theprogesterone is produced by corpus luteum (ovaries), which triggers the production of FSH and LH. There are many types of progesterone available.Long-term usage of synthetic estrogen and progesterone can disturb the balance between the level of these hormones in the body. This imbalance maylead to severe side effects such as breast cancer, cervical cancer, thrombosis, direct impact on the brain, and infertility.Keywords: Estrogen, Progesterone, Contraceptives, Herbal contraceptives.

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Chesnokova, Vera, and Shlomo Melmed. "Peptide Hormone Regulation of DNA Damage Responses." Endocrine Reviews 41, no. 4 (April 9, 2020): 519–37. http://dx.doi.org/10.1210/endrev/bnaa009.

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Abstract DNA damage response (DDR) and DNA repair pathways determine neoplastic cell transformation and therapeutic responses, as well as the aging process. Altered DDR functioning results in accumulation of unrepaired DNA damage, increased frequency of tumorigenic mutations, and premature aging. Recent evidence suggests that polypeptide hormones play a role in modulating DDR and DNA damage repair, while DNA damage accumulation may also affect hormonal status. We review the available reports elucidating involvement of insulin-like growth factor 1 (IGF1), growth hormone (GH), α-melanocyte stimulating hormone (αMSH), and gonadotropin-releasing hormone (GnRH)/gonadotropins in DDR and DNA repair as well as the current understanding of pathways enabling these actions. We discuss effects of DNA damage pathway mutations, including Fanconi anemia, on endocrine function and consider mechanisms underlying these phenotypes. (Endocrine Reviews 41: 1 – 19, 2020)

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Deventhiran, Radhakrishnan, Kumaresan Ramanathan, and Nagamurugan Nandakumar. "PREVALANCE OF MALE INFERTILITY IN INDIA: STUDIES ON THE EFFECTS OF GONADOTROPIN RELEASING HORMONES." Asian Journal of Pharmaceutical and Clinical Research 10, no. 8 (August 1, 2017): 208. http://dx.doi.org/10.22159/ajpcr.2017.v10i8.18254.

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Objective: Nowadays, there is an increased incidence of infertility in Indian males due to lifestyle changes. Hence, the objective of this study isevaluating the gonadotropin releasing hormones (GnRH) level in infertile young male in Indian population.Materials and Methods: In total, 56 patients having abnormal semen count and five control patients have been included in the study. All patientswere underwent sperm count and estimation of hormones includes GnRH such as follicle stimulating hormone (FSH), tri-iodothyronine, thyroxin,prolactin, and testosterone.Results: The sperm concentration of infertile men was significantly lower than control. Sperm motility behaviors rapid, sluggish, and non-motilecharacters were significantly lower than control. Among GnRH, FSH has been significantly higher in infertile group than control group.Conclusion: FSH may be considered as a marker for male infertility.

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Gavin, Kathleen M., Karen L. Shea, Ellie Gibbons, Pamela Wolfe, Robert S. Schwartz, Margaret E. Wierman, and Wendy M. Kohrt. "Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone." American Journal of Physiology-Endocrinology and Metabolism 315, no. 2 (August 1, 2018): E316—E325. http://dx.doi.org/10.1152/ajpendo.00221.2017.

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Sex hormones appear to play a role in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity. The objective was to isolate the effects of estradiol (E2) on central activation of the HPA axis. We hypothesized that the HPA axis response to corticotropin-releasing hormone (CRH) under dexamethasone (Dex) suppression would be exaggerated in response to chronic ovarian hormone suppression and that physiologic E2 add-back would mitigate this response. Thirty premenopausal women underwent 20 wk of gonadotropin-releasing hormone agonist therapy (GnRHAG) and transdermal E2 (0.075 mg per day, GnRHAG + E2, n = 15) or placebo (PL) patch (GnRHAG + PL, n = 15). Women in the GnRHAG + PL and GnRHAG + E2 groups were of similar age (38 (SD 5) yr vs. 36 (SD 7) yr) and body mass index (27 (SD 6) kg/m2 vs. 27 (SD 6) kg/m2). Serum E2 changed differently between the groups ( P = 0.01); it decreased in response to GnRHAG + PL (77.9 ± 17.4 to 23.2 ± 2.6 pg/ml; P = 0.008) and did not change in response to GnRHAG + E2 (70.6 ± 12.4 to 105 ± 30.4 pg/ml; P = 0.36). The incremental area under the curve (AUCINC) responses to CRH were different between the groups for total cortisol ( P = 0.03) and cortisone ( P = 0.04) but not serum adrenocorticotropic hormone (ACTH) ( P = 0.28). When examining within-group changes, GnRHAG + PL did not alter the HPA axis response to Dex/CRH, but GnRHAG + E2 decreased the AUCINC for ACTH (AUCINC, 1,623 ± 257 to 1,211 ± 236 pg/ml·min, P = 0.004), cortisone (1,795 ± 367 to 1,090 ± 281 ng/ml·min, P = 0.009), and total cortisol (7,008 ± 1,387 to 3,893 ± 1,090 ng/ml·min, P = 0.02). Suppression of ovarian hormones by GnRHAG therapy for 20 wk did not exaggerate the HPA axis response to CRH, but physiologic E2 add-back reduced HPA axis activity compared with preintervention levels.

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Pant, Dinesh Raj, and Pooja Kumari. "Effect of exogenously administered thyroid hormones on gonadotropin, thyrotropin and deiodinases encoding genes in the catfish, Heteropneustes fossilis (Bloch)." Environment Conservation Journal 24, no. 1 (February 11, 2023): 261–66. http://dx.doi.org/10.36953/ecj.17222519.

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Thyroid hormones are known to regulate the basal metabolism rate of an organism. They are also known to regulate the seasonal reproduction of long-day breeding vertebrates in response to thyrotropin induced deiodinase enzymes switching in the brain. The current study attempted to investigate the effect of intraperitoneal administration of thyroxine (T4) and tri-iodothyronine (T3) hormones at various doses on gonadal recrudescence, plasma estradiol-17β and quantitative expression analysis of genes encoding for gonadotropin, thyrotropin, and deiodinases. The estradiol-17β levels were not affected by either thyroid hormone; however, the gonado-somatic index (GSI) and ovarian histology were varying. The gonadotropin releasing hormone 2 (gnrh2) and follicle stimulating hormone-β subunit (fsh-b) gene expressions correspond to the fish GSI and ovarian histology. The gene expressions show that T4 inhibits the expression of thyroid stimulating hormone-β subunit (tsh-b) and type 3 deiodinase (dio3), though it enhances the expression of type 2 deiodinase (dio2). T3, on the other hand, inhibits tsh-b and dio2 expression while increasing dio3 expression. In summary, the T4 appears to regulate gonadal recrudescence in Heteropneustes fossilis in a dose-dependent manner, whereas the T3 appears to have no effect on gonadal activity.

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Agarwal, Ashish, Anupama Hegde, Afzal Ahmad, Charu Yadav, Poornima A. Manjrekar, and Rukmini M.S. "Assessment of endocrine function in males with pre-diabetes." Biomedicine 43, no. 5 (November 8, 2023): 1430–35. http://dx.doi.org/10.51248/.v43i5.3643.

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Introduction and Aim: Diabetes mellitus is associated with various endocrine derangements and prediabetes is an intermediate condition between health and full-fledged disease state. Hormones of Hypothalamus-Pituitary-Thyroid (HPT), Hypothalamus-Pituitary-Adrenal (HPA), Hypothalamus-Pituitary-Gonadal (HPG) axes and pineal gland were studied in males (n=105) with prediabetes. Materials and Methods: Based on fasting plasma glucose (FPG), the subjects were categorized as healthy controls, prediabetes, diabetes and various hormones were compared between these three groups. Results: Insulin levels showed a systematic increase from pre-diabetes to diabetes subjects. HPT axis had a semblance to “Primary hypothyroidism” with an increase in Thyrotropin-releasing-hormone (TRH), Thyroid-stimulating-hormone (TSH) and decrease in fT4 and fT3 with rise in glucose levels. HPA axis detected high Corticotropin Releasing Hormone (CRH), Adrenocorticotropic hormone (ACTH), cortisol in the overtly diabetic group while prediabetes values were comparable to control. The HPG axis demonstrated significantly high Gonadotropin-hormone-releasing-hormone (GnRH) in the diabetic group but not in the prediabetic. A graded increase in LH and significant decrease in testosterone and melatonin was observed with a rise in FPG. Conclusion: Thus, it could be concluded as endocrine gland damage due to hyperglycemia and hyperinsulinemia causes multiple endocrine dysfunctions in prediabetes that aggravates, as the patient turns diabetic.

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NAOR, ZVI. "Signal Transduction Mechanisms of Ca2+Mobilizing Hormones: The Case of Gonadotropin-Releasing Hormone*." Endocrine Reviews 11, no. 2 (May 1990): 326–53. http://dx.doi.org/10.1210/edrv-11-2-326.

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Zerani, Massimo, Alberta Polzonetti‐Magni, Anna Gobbetti, Oliana Carnevali, and Virgilio Botte. "Effects of gonadotropin‐releasing hormone on plasma sex hormones inrana esculenta. in vivostudies." Bolletino di zoologia 58, no. 1 (January 1991): 77–79. http://dx.doi.org/10.1080/11250009109355731.

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Malik, Minnie, Joy Britten, Jeris Cox, Amrita Patel, and William H. Catherino. "Gonadotropin-releasing hormone analogues inhibit leiomyoma extracellular matrix despite presence of gonadal hormones." Fertility and Sterility 105, no. 1 (January 2016): 214–24. http://dx.doi.org/10.1016/j.fertnstert.2015.09.006.

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Parveen, Gulshan, Ali Hassan, Muhammad Hassam Rehm, Awais Altaf, Nureen Zahra, Arif Malik, Anam Naz, and Huma Sattar. "Circulating Expressions of Gonadotropin Releasing Hormones and Risk of Ovarian Cancer." Pakistan Journal of Medical and Health Sciences 15, no. 11 (November 30, 2021): 3372–75. http://dx.doi.org/10.53350/pjmhs2115113372.

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Background: Ovarian cancer (OC) is a worst type of malignancy in the field of gynecology. This is because ovarian tumors diagnosed at advanced stage of disease. The exact mechanism for its development is still unknown. Aim: The aim of this study is to measure the levels of steroidal hormones and their function in ovarian cancer progression. Methods: In the present study, fifty ovarian cancer patients and fifty control individuals were taken and serum was separated from their blood samples. The levels of steroid hormones were measured by ELISA kit methods. Results: Result of the current study determined the levels of E2, progesterone, testosterone, FSH, LH, 17-β-HSD-I, 17-β-HSD-II, cortisol and aromatase were extensively higher in patient group in comparison with healthy individuals. Conclusion: Current study concluded the Study concluded that overexpression of steroid hormones may lead to enhance tumor survival in ovarian cancer through various signaling mechanisms. Keywords: Ovarian cancer, Estradiol, FSH, LH, progesterone

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Toth, Michael J., Cynthia K. Sites, Dwight E. Matthews, and Peter R. Casson. "Ovarian suppression with gonadotropin-releasing hormone agonist reduces whole body protein turnover in women." American Journal of Physiology-Endocrinology and Metabolism 291, no. 3 (September 2006): E483—E490. http://dx.doi.org/10.1152/ajpendo.00600.2005.

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The age-related decline in fat-free mass is accelerated in women after menopause. The role of ovarian hormone deficiency in the regulation of fat-free mass, however, has not been clearly defined. To address this question, we examined the effect of ovarian hormone suppression on whole body protein metabolism. Whole body protein breakdown, oxidation, and synthesis were measured using [13C]leucine in young, healthy women with regular menstrual patterns before and after 2 mo of treatment with gonadotropin-releasing hormone agonist (GnRHa; n = 6) or placebo ( n = 7). Protein metabolism was measured under postabsorptive and euglycemic-hyperinsulinemic-hyperaminoacidemic conditions. Ovarian suppression did not alter whole body or regional fat-free mass or adiposity. In the postabsorptive state, GnRHa administration was associated with reductions in protein breakdown and synthesis ( P < 0.05), whereas no change in protein oxidation was noted. Under euglycemic-hyperinsulinemic-hyperaminoacidemic conditions, a similar reduction ( P < 0.05) in protein synthesis and breakdown was noted, whereas, protein oxidation increased ( P < 0.05) in the placebo group. Testosterone, steroid hormone precursors, insulin-like growth factor I, and their respective binding proteins were not altered by GnRHa administration, and changes in these hormones over time were not associated with GnRHa-induced alterations in protein metabolism, suggesting that changes in protein turnover are not due to an effect of ovarian suppression on other endocrine systems. Our findings provide evidence that endogenous ovarian hormones participate in the regulation of protein turnover in women.

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43

Seong, Jae Young, and Hyuk Bang Kwon. "Molecular co‐evolution of Gonadotropin‐releasing hormones and their receptors." Integrative Biosciences 11, no. 2 (January 2007): 93–98. http://dx.doi.org/10.1080/17386357.2007.9647320.

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Millar, RP, PJ Wormald, and RC Milton. "Stimulation of gonadotropin release by a non-GnRH peptide sequence of the GnRH precursor." Science 232, no. 4746 (April 4, 1986): 68–70. http://dx.doi.org/10.1126/science.3082009.

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The human gonadotropin-releasing hormone (GnRH) precursor comprises the GnRH sequence followed by an extension of 59 amino acids. Basic amino acid residues in the carboxyl terminal extension may represent sites of processing to biologically active peptides. A synthetic peptide comprising the first 13 amino acids (H X Asp-Ala-Glu-Asn-Leu-Ile-Asp-Ser-Phe-Gln-Glu-Ile-Val X OH) of the 59-amino acid peptide was found to stimulate the release of gonadotropic hormones from human and baboon anterior pituitary cells in culture. The peptide did not affect thyrotropin or prolactin secretion. A GnRH antagonist did not inhibit gonadotropin stimulation by the peptide, and the peptide did not compete with GnRH for GnRH pituitary receptors, indicating that the action of the peptide is independent of the GnRH receptor. The GnRH precursor contains two distinct peptide sequences capable of stimulating gonadotropin release from human and baboon pituitary cells.

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Hu, Kaili, Wenyan Sun, Yu Li, Bo Zhang, Meng Zhang, Chunyan Guo, HongSheng Chang, and Xiaoling Wang. "Study on the Mechanism of Sarsasapogenin in Treating Precocious Puberty by Regulating the HPG Axis." Evidence-Based Complementary and Alternative Medicine 2020 (August 5, 2020): 1–10. http://dx.doi.org/10.1155/2020/1978043.

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The present study aims to investigate the effects and mechanisms of sarsasapogenin resistance to precocious puberty. Female Sprague Dawley rats were divided into a normal (N) group, model (M) group, leuprolide (L) group, and sarsasapogenin (Sar) group. Rats at 5 days of age were given a single subcutaneous injection of 300 micrograms of danazol to establish the precocious puberty model. After 10 days of modeling, drug intervention was started. The development of the uterus and ovary was observed by hematoxylin and eosin (HE) staining. The levels of the serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol (E2) were determined by radioimmunoassay. Also, the expressions of the hypothalamic gonadotropin releasing hormone (GnRH), Kiss-1, G protein-coupled receptor 54 (GPR54), and pituitary gonadotropin releasing hormone receptor (GnRH-R) were detected by RT-PCR. The results showed that compared with the model group, sarsasapogenin could significantly delay the opening time of vaginal, decreased uterine and ovarian coefficients, and reduced uterine wall thickness. Moreover, it can significantly downregulate the levels of serum hormones and reduce the expression of GnRH, GnRH-R, and kiss-1. In summary, our results indicate that sarsasapogenin can regulate the HPG axis through the kiss-1/GPR54 system for therapeutic precocious puberty.

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Siler-Khodr, T. M., G. S. Khodr, G. Valenzuela, and J. Rhode. "Gonadotropin-releasing Hormone Effects on Placental Hormones during Gestation: I. Alpha-Human Chorionic Gonadotropin, Human Chorionic Gonadotropin and Human Chorionic Somatomammotropin." Biology of Reproduction 34, no. 2 (March 1, 1986): 245–54. http://dx.doi.org/10.1095/biolreprod34.2.245.

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Ceccatelli, S., A. L. Hulting, X. Zhang, L. Gustafsson, M. Villar, and T. Hökfelt. "Nitric oxide synthase in the rat anterior pituitary gland and the role of nitric oxide in regulation of luteinizing hormone secretion." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 11292–96. http://dx.doi.org/10.1073/pnas.90.23.11292.

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By using immunohistochemistry and in situ hybridization, we have demonstrated that the nitric oxide (NO)-synthesizing enzyme NO synthase is present in gonadotrophs and in folliculo-stellate cells of the anterior pituitary gland of male and female rats. A marked increase in levels of NO synthase protein and mRNA was observed after gonadectomy. In vitro studies on dispersed anterior pituitary cells suggest that NO inhibits gonadotropin-releasing-hormone-stimulated luteinizing hormone release. An inhibitory effect of NO has also been shown on growth-hormone-releasing-hormone-stimulated release of growth hormone [Kato, M. (1992) Endocrinology 131, 2133-2138]. Thus these findings support a dual mechanism for NO in the control of anterior pituitary hormone secretion, an autocrine mediation of luteinizing hormone release on gonadotrophs, and a paracrine effect on growth hormone secretion involving folliculo-stellate cells closely related to somatotrophs. We speculate that NO may participate in producing the pulsatile secretion patterns of these two pituitary hormones.

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Acampora, D., S. Mazan, F. Tuorto, V. Avantaggiato, J. J. Tremblay, D. Lazzaro, A. di Carlo, et al. "Transient dwarfism and hypogonadism in mice lacking Otx1 reveal prepubescent stage-specific control of pituitary levels of GH, FSH and LH." Development 125, no. 7 (April 1, 1998): 1229–39. http://dx.doi.org/10.1242/dev.125.7.1229.

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Genetic and molecular approaches have enabled the identification of regulatory genes critically involved in determining cell types in the pituitary gland and/or in the hypothalamus. Here we report that Otx1, a homeobox-containing gene of the Otx gene family, is postnatally transcribed and translated in the pituitary gland. Cell culture experiments indicate that Otx1 may activate transcription of the growth hormone (GH), follicle-stimulating hormone (betaFSH), luteinizing hormone (betaLH) and alpha-glycoprotein subunit (alphaGSU) genes. Analysis of Otx1 null mice indicates that, at the prepubescent stage, they exhibit transient dwarfism and hypogonadism due to low levels of pituitary GH, FSH and LH hormones which, in turn, dramatically affect downstream molecular and organ targets. Nevertheless, Otx1−/− mice gradually recover from most of these abnormalities, showing normal levels of pituitary hormones with restored growth and gonadal function at 4 months of age. Expression patterns of related hypothalamic and pituitary cell type restricted genes, growth hormone releasing hormone (GRH), gonadotropin releasing hormone (GnRH) and their pituitary receptors (GRHR and GnRHR) suggest that, in Otx1−/− mice, hypothalamic and pituitary cells of the somatotropic and gonadotropic lineages appear unaltered and that the ability to synthesize GH, FSH and LH, rather than the number of cells producing these hormones, is affected. Our data indicate that Otx1 is a new pituitary transcription factor involved at the prepubescent stage in the control of GH, FSH and LH hormone levels and suggest that a complex regulatory mechanism might exist to control the physiological need for pituitary hormones at specific postnatal stages.

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Choi, Young Jae, Seul Gi Na Ra Park, A.-Hyun Jo, and Jun-Hwan Kim. "Physiological Effect of Extended Photoperiod and Green Wavelength on the Pituitary Hormone, Sex Hormone and Stress Response in Chub Mackerel, Scomber japonicus." Fishes 8, no. 2 (January 29, 2023): 77. http://dx.doi.org/10.3390/fishes8020077.

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Chub mackerel, Scomber japonicus, is heavily farmed and harvested due to its demand as a high-quality protein source rich in fatty acids. However, the effects of environmental cues on sexual maturation of the fish remain understudied. We aim to elucidate the effect of light manipulation on the hormones related to reproduction and on the stress response in the species. Mackerel were exposed to different photoperiods (12 h light:12 h dark or 14 h light:10 h dark) and light wavelengths (provided by white fluorescent bulbs or green LEDs). Total RNA extracted from the brain was assayed with quantitative polymerase chain reaction (a powerful technique for advancing functional genomics) and blood plasma was analyzed via immunoassay using ELISA kits. The mRNA expression of gene-encoding gonadotropin-releasing hormone, gonadotropin hormone, follicle-stimulating hormone, and luteinizing hormone were significantly increased through the use of an extended photoperiod and green wavelength, which also increased testosterone and 17β-estradiol plasma levels. Plasma levels of cortisol and glucose, which are indicators of a stress response, were significantly decreased through green LED exposure. Our results indicate that environmental light conditions affect the production of pituitary and sex hormones, and reduce the stress response in S. japonicus.

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Wan, Boyang, Xuejun Yuan, Weiren Yang, Ning Jiao, Yang Li, Faxiao Liu, Mei Liu, Zaibin Yang, Libo Huang, and Shuzhen Jiang. "The Effects of Zearalenone on the Localization and Expression of Reproductive Hormones in the Ovaries of Weaned Gilts." Toxins 13, no. 9 (September 7, 2021): 626. http://dx.doi.org/10.3390/toxins13090626.

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This study aims to investigate the effects of zearalenone (ZEA) on the localizations and expressions of follicle stimulating hormone receptor (FSHR), luteinizing hormone receptor (LHR), gonadotropin releasing hormone (GnRH) and gonadotropin releasing hormone receptor (GnRHR) in the ovaries of weaned gilts. Twenty 42-day-old weaned gilts were randomly allocated into two groups, and treated with a control diet and a ZEA-contaminated diet (ZEA 1.04 mg/kg), respectively. After 7-day adjustment, gilts were fed individually for 35 days and euthanized for blood and ovarian samples collection before morning feeding on the 36th day. Serum hormones of E2, PRG, FSH, LH and GnRH were determined using radioimmunoassay kits. The ovaries were collected for relative mRNA and protein expression, and immunohistochemical analysis of FSHR, LHR, GnRH and GnRHR. The results revealed that ZEA exposure significantly increased the final vulva area (p < 0.05), significantly elevated the serum concentrations of estradiol, follicle stimulating hormone and GnRH (p < 0.05), and markedly up-regulated the mRNA and protein expressions of FSHR, LHR, GnRH and GnRHR (p < 0.05). Besides, the results of immunohistochemistry showed that the immunoreactive substances of ovarian FSHR, LHR, GnRH and GnRHR in the gilts fed the ZEA-contaminated diet were stronger than the gilts fed the control diet. Our findings indicated that dietary ZEA (1.04 mg/kg) could cause follicular proliferation by interfering with the localization and expression of FSHR, LHR, GnRH and GnRHR, and then affect the follicular development of weaned gilts.

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Journal articles on the topic 'Gonadotropin-Releasing hormones'

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