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Literatura académica sobre el tema "Preovulatory luteinizing hormone surge"

Autor: Grafiati

Publicado: 29 de marzo de 2025

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Artículos de revistas sobre el tema "Preovulatory luteinizing hormone surge"

Rangel, P. L., P. J. Sharp y C. G. Gutierrez. "Testosterone antagonist (flutamide) blocks ovulation and preovulatory surges of progesterone, luteinizing hormone and oestradiol in laying hens". Reproduction 131, n.º 6 (junio de 2006): 1109–14. http://dx.doi.org/10.1530/rep.1.01067.

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The preovulatory release of luteinizing hormone (LH) in the domestic hen occurs after the initiation of a preovulatory surge of testosterone. The objective of this study was to determine whether this testosterone surge has functional significance in the endocrine control of ovulation. Groups of laying hens (n=10–22) were treated with the androgen receptor antagonist, flutamide, at 8 h intervals for 24 h at doses of 0, 31.25, 62.5, 125 and 250 mg. All doses reduced egg laying (P < 0.001), with the highest dose being the most effective. In a second study, laying hens (n=9) were treated with 250 mg flutamide at 8 h intervals for 24 h with a control group being given placebo (n=10). Blood samples were taken for hormone measurements at 2 h intervals for 18 h starting 4 h before the onset of darkness. The percentage of hens laying per day did not differ between groups before treatment (control, 88% vs flutamide, 86%). Ovulation was blocked in all hens treated with flutamide within 2 days while the control hens continued to lay at the pretreatment rate (80%). Preovulatory surges of plasma testosterone, progesterone, oestradiol and LH were observed in control hens but with the exception of testosterone, flutamide treatment blocked the progesterone, oestradiol and LH surges. LH concentrations declined progressively with time in the flutamide-treated hens. It is concluded that inhibition of testosterone action blocks egg laying and the preovulatory surges of progesterone, luteinizing hormone and oestradiol demonstrating a key role for the preovulatory release of testosterone in the endocrine control of ovulation in the domestic hen.

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Zheng, Cuihong, Thippeswamy Gulappa, Bindu Menon y K. M. J. Menon. "Association between LH receptor regulation and ovarian hyperstimulation syndrome in a rodent model". Reproduction 160, n.º 2 (agosto de 2020): 239–45. http://dx.doi.org/10.1530/rep-20-0058.

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Ovarian hyperstimulation syndrome (OHSS) is a common complication of ovarian stimulation associated with the administration of human chorionic gonadotropin (hCG) during assisted reproduction. We have determined the expression of luteinizing hormone receptor (Lhcgr) mRNA, vascular endothelial growth factor (VEGF), and its transcription factor, HIF1α, during the periovulatory period in a rodent model of OHSS and compared these results with normal ovulatory periods. These results showed that the downregulation of Lhcgr mRNA in response to conditions that mimic preovulatory LH surge was significantly impaired in the OHSS group compared to the complete downregulation seen in the control group. Most importantly, the downregulation of luteinizing hormone receptor mRNA expression following hCG administration was sustained in the control group up to 48 h, whereas it remained at significantly higher levels in the OHSS group. This impairment of hCG-induced Lhcgr downregulation in the OHSS group was accompanied by significantly elevated levels of VEGF and its transcription factor, HIF1α. Furthermore, the downregulation of Lhcgr that occurs in response to a preovulatory LH surge in normal cycles was accompanied by low levels of VEGF. This study shows that, while downregulation of Lhcgr as well as low VEGF levels are seen in response to a preovulatory LH surge in normal ovarian cycle, impaired Lhcgr downregulation and elevated VEGF levels were found in the OHSS group.

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Bowen, Jennifer M., Geoffrey E. Dahl, Neil P. Evans, Lori A. Thrun, Yuedong Wang, Morton B. Brown y Fred J. Karsch. "Importance of the Gonadotropin-Releasing Hormone (GnRH) Surge for Induction of the Preovulatory Luteinizing Hormone Surge of the Ewe: Dose-Response Relationship and Excess of GnRH*". Endocrinology 139, n.º 2 (1 de febrero de 1998): 588–95. http://dx.doi.org/10.1210/endo.139.2.5719.

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Abstract The preovulatory LH surge in the ewe is stimulated by a large sustained surge of GnRH. We have previously demonstrated that the duration of this GnRH signal exceeds that necessary to initiate and sustain the LH surge. The objective of the present study was to determine whether a similar excess exists for amplitude of the GnRH surge. Experiments were performed using an animal model in which GnRH secretion was blocked by progesterone, which in itself does not block the pituitary response to GnRH. To assess the amplitude of the GnRH surge needed to induce the LH surge, we introduced artificial GnRH surges of normal contour and duration but varying amplitudes. Twelve ewes were run through 3 successive artificial follicular phases (total of 36). Six of these artificial follicular phases were positive controls, in which progesterone was removed, the estradiol stimulus was provided, and vehicle was infused. In these control cycles, animals generated endogenous LH surges. In the remaining artificial follicular phases, progesterone was not withdrawn, the estradiol stimulus was provided, and either vehicle (negative control) or GnRH solutions of varying concentrations (experimental) were infused. The circulating GnRH concentrations achieved by infusion were monitored. No LH surges were observed in negative controls, whereas LH surges were induced in experimental cycles provided a sufficient dose of GnRH was infused. A highly significant dose-response relationship was observed between the amplitude of the GnRH surge and both the amplitude of the LH surge and the area under the curve describing the LH response, but no such relationship existed between the amplitude of the GnRH surge and the duration of the LH response. In numerous cases, LH surges similar to those in the positive control animals resulted from infusion of amounts of GnRH estimated to be considerably less than those delivered to the pituitary during the endogenously generated GnRH/LH surge. These findings indicate that, in the ewe, increased GnRH secretion drives the preovulatory LH surge in a dose-dependent fashion, and they provide evidence that the amplitude of the GnRH surge may exceed that needed to generate the LH surge.

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Choi, Yuri, Okto Lee, Kiyoung Ryu y Jaesook Roh. "Luteinizing Hormone Surge-Induced Krüppel-like Factor 4 Inhibits Cyp17A1 Expression in Preovulatory Granulosa Cells". Biomedicines 12, n.º 1 (27 de diciembre de 2023): 71. http://dx.doi.org/10.3390/biomedicines12010071.

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Previous in vivo and in vitro studies have demonstrated a dramatic up-regulation of Krüppel-like factor 4 (Klf4) in rat preovulatory granulosa cells (GCs) after LH/hCG treatment and its role in regulating Cyp19A1 expression during the luteal shift in steroidogenesis. In this study, we examined whether Klf4 also mediates the LH-induced repression of Cyp17A1 expression in primary rat preovulatory GCs. In response to LH treatment of GCs in vitro, Cyp17A1 expression declined to less than half of its initial value by 1 h, remaining low for 24 h of culture. Overexpression of Klf4 decreased basal and Sf1-induced Cyp17A1 expressions and increased progesterone secretion. Reduction of endogenous Klf4 by siRNA elevated basal Cyp17A1 expression but did not affect LH-stimulated progesterone production. Overexpression of Klf4 also significantly attenuated Sf1-induced Cyp17A1 promoter activity. On the other hand, mutation of the conserved Sp1/Klf binding motif in the promoter revealed that this motif is not required for Klf4-mediated repression. Taken together, these data indicate that the Cyp17A1 gene may be one of the downstream targets of Klf4, which is induced by LH in preovulatory GCs. This information may help in identifying potential targets for preventing the molecular changes occurring in hyperandrogenic disorders.

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Matsuwaki, T., M. Suzuki, K. Yamanouchi y M. Nishihara. "Glucocorticoid counteracts the suppressive effect of tumor necrosis factor-alpha on the surge of luteinizing hormone secretion in rats". Journal of Endocrinology 181, n.º 3 (1 de junio de 2004): 509–13. http://dx.doi.org/10.1677/joe.0.1810509.

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We have previously reported that tumor necrosis factor-alpha (TNF-alpha) suppressed pulsatile secretion of luteinizing hormone (LH) in adrenalectomized (ADX) rats, which was restored by replacement of glucocorticoid. In the present study, we examined the role of glucocorticoid in inducing the preovulatory LH surge under conditions of infectious stress. Intravenous injection of TNF-alpha (1 microg) into the proestrous rats at 1300 h attenuated the LH surge and decreased the number of oocytes ovulated. The inhibitory effect of TNF-alpha on the LH surge was blocked by pretreatment with indomethacin, suggesting that the effects of TNF-alpha were mediated by prostaglandins (PGs). On the other hand, ADX markedly enhanced the inhibitory effect of TNF-alpha on the LH surge and subsequent ovulation, which was almost completely restored by pretreatment with a subcutaneous injection of corticosterone (10 mg). These results suggest that glucocorticoid counteracts the inhibitory effect of the cytokines on the preovulatory LH surge by suppressing PG synthesis, and thereby helps to maintain reproductive function under infectious stress conditions.

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Morello, H., L. Caligaris, B. Haymal y S. Taleisnik. "Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats". Canadian Journal of Physiology and Pharmacology 70, n.º 4 (1 de abril de 1992): 447–51. http://dx.doi.org/10.1139/y92-057.

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Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light: dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of γ-aminobutyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.Key words: serotonin, GABA, proestrous LH surge, ovulation, median raphe nucleus, daily rhythms.

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da Silva Bitecourt, Frederico, Carina Oliveira Dumont Horta, Karen Santos Lima, Bruno Bastos Godoi, Fernanda Luiza Menezes Bello, Cíntia Maria Rodrigues, Luana Pereira Leite Schetino y Kinulpe Honorato-Sampaio. "Morphological study of apoptosis in granulosa cells and ovulation in a model of atresia in rat preovulatory follicles". Zygote 26, n.º 4 (agosto de 2018): 336–41. http://dx.doi.org/10.1017/s0967199418000291.

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SummaryPrevious studies have established a model of atresia in preovulatory follicles after stimulation of immature rats with equine chorionic gonadotropin (eCG). This gonadotropin recruits a follicular pool and the deprivation of preovulatory luteinizing hormone (LH) surge induces the atresia in preovulatory follicles. The present study investigated the occurrence of ovulation and provided some morphological features of granulosa cell (GC) apoptosis of atretic follicles at 0, 48, 72 and 120 h after eCG stimulation. Histological sections of ovaries from untreated animals (0 h) showed primordial, primary, secondary and early antral follicles. After 48 h ovaries showed large antral follicles. Preovulatory follicles were observed at 72 h, and two out of five rats displayed cumulus–oocyte complexes (COCs) in the oviducts. All animals exhibited corpora lutea after 120 h. We observed increased estradiol (E2) levels 48 h after eCG treatment that might trigger an endogenous preovulatory gonadotropin surge. Higher progesterone (P4) level, which is the hallmark of a functional corpus luteum, was observed at 120 h. Atresia in secondary and antral follicles was observed by pyknotic granulosa cell nuclei in histology and positive immunolabelling for cleaved caspase 3. We also observed macrophages in secondary and antral follicles in atresia. Transmission electron microscopy revealed GCs with compacted chromatin against the nuclear envelope, nuclear fragmentation, cell shrinkage and fragmentation. No preovulatory follicles showed apoptosis of GCs. In conclusion, our results suggested the occurrence of an endogenous gonadotropin surge, promoting ovulation and preventing atresia of preovulatory follicles.

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Roozendaal, Marjolijn M., Hans JM Swarts, Victor M. Wiegant y John AM Mattheij. "Effect of restraint stress on the preovulatory luteinizing hormone profile and ovulation in the rat". European Journal of Endocrinology 133, n.º 3 (septiembre de 1995): 347–53. http://dx.doi.org/10.1530/eje.0.1330347.

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Roozendaal MM, Swarts HJM, Wiegant VM, Mattheij JAM. Effect of restraint stress on the preovulatory luteinizing hormone profile and ovulation in the rat. Eur J Endocrinol 1995;133:347–53. ISSN 0804–4643 Plasma profiles of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured during restraint stress on the day of pro-oestrus; these profiles were considered in relation to ovulation rate on the next day. Rats bearing a permanent jugular vein cannula were subjected to restraint, which was started 0, 1 or 2 h before the presumed onset of the LH surge and ended just before the beginning of the dark period. Exposure to restraint resulted in a suppression of the secretion of both gonadotrophins on the day of pro-oestrus. Suppression of the LH surge was virtually complete (plasma LH ≤ 0.2 ng/ml) in 15 out of 32 stressed rats, and the ovaries of these rats contained graafian follicles with oocytes in germinal vesicle stage. In these rats, the LH surge did not occur 24 h later. In the remaining 17 rats, restraint resulted in a considerable suppression of the LH surge. Of these rats, five had an ovulation rate of 100% and four ovulated partially. In unruptured follicles of the latter, the oocyte had not resumed meiosis and the follicle wall was not luteinized. In the remaining eight rats with a reduced LH surge, ovulations had not occurred and graafian follicles were unaffected. The results of this study indicate that during pro-oestrus restraint stress suppresses and does not delay the release of preovulatory gonadotrophins. Partial suppression of LH by restraint does not result in induction of meiotic resumption without subsequent ovulation or in luteinized unruptured follicles. JAM Mattheij, Department of Human and Animal Physiology, Agricultural University, Haarweg 10, 6709 PJ, Wageningen, The Netherlands

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Chu, Adrienne, Lei Zhu, Ian D. Blum, Oliver Mai, Alexei Leliavski, Jan Fahrenkrug, Henrik Oster, Ulrich Boehm y Kai-Florian Storch. "Global But Not Gonadotrope-Specific Disruption of Bmal1 Abolishes the Luteinizing Hormone Surge Without Affecting Ovulation". Endocrinology 154, n.º 8 (1 de agosto de 2013): 2924–35. http://dx.doi.org/10.1210/en.2013-1080.

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Abstract Although there is evidence for a circadian regulation of the preovulatory LH surge, the contributions of individual tissue clocks to this process remain unclear. We studied female mice deficient in the Bmal1 gene (Bmal1−/−), which is essential for circadian clock function, and found that they lack the proestrous LH surge. However, spontaneous ovulation on the day of estrus was unaffected in these animals. Bmal1−/− females were also deficient in the proestrous FSH surge, which, like the LH surge, is GnRH-dependent. In the absence of circadian or external timing cues, Bmal1−/− females continued to cycle in constant darkness albeit with increased cycle length and time spent in estrus. Because pituitary gonadotropes are the source of circulating LH and FSH, we assessed hypophyseal circadian clock function and found that female pituitaries rhythmically express clock components throughout all cycle stages. To determine the role of the gonadotrope clock in the preovulatory LH and FSH surge process, we generated mice that specifically lack BMAL1 in gonadotropes (GBmal1KO). GBmal1KO females exhibited a modest elevation in both proestrous and baseline LH levels across all estrous stages. BMAL1 elimination from gonadotropes also led to increased variability in estrous cycle length, yet GBmal1KO animals were otherwise reproductively normal. Together our data suggest that the intrinsic clock in gonadotropes is dispensable for LH surge regulation but contributes to estrous cycle robustness. Thus, clocks in the suprachiasmatic nucleus or elsewhere must be involved in the generation of the LH surge, which, surprisingly, is not required for spontaneous ovulation.

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Hatanaka, Fumiko y Masaru Wada. "Mechanism controlling photostimulated luteinizing hormone secretion is different from preovulatory luteinizing hormone surge in Japanese quail (Coturnix coturnix japonica)". General and Comparative Endocrinology 70, n.º 1 (abril de 1988): 101–8. http://dx.doi.org/10.1016/0016-6480(88)90098-6.

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Tesis sobre el tema "Preovulatory luteinizing hormone surge"

Simonneaux, Marine. "Évaluation de l’impact de la perturbation du rythme circadien sur la fonction de reproduction des mammifères femelles". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ096.

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Chez les mammifères femelles, une fertilité optimale repose sur la synchronisation des évènements neuroendocriniens et comportementaux régulant la fonction de reproduction. Pour cela, l’horloge circadienne principale, entrainée par l’alternance lumière/obscurité, rythme l’axe hypothalamo-hypophyso-ovarien. Ainsi, des cycles jour/nuit irréguliers, comme lors du travail en horaires décalés, peuvent altérer la fonction de reproduction et diminuer la fertilité, notamment chez les femmes. Ce travail de recherche visait à évaluer les effets de la perturbation du rythme circadien sur la fonction de reproduction féminine et à étudier les mécanismes neuroendocriniens sous-jacents. Chez la souris femelles, l’exposition à un décalage horaire chronique a entrainé une désynchronisation majeure du pic préovulatoire de LH, persistant plusieurs semaines. Cette altération était associée à une modification de la transmission de l’information journalière de l’horloge principale aux neurones à kisspeptine qui régulent la sécrétion de LH. De plus, la capacité reproductive des souris était diminuée, mais sans effet majeur sur le développement de leur descendance
In female mammals, optimal fertility relies on the synchronization of neuroendocrine and behavioral events regulating reproductive function. To this end, the circadian timing system, entrained by the light-dark cycle, sets the pace for the hypothalamic-pituitary-ovarian axis. Therefore, irregular light-dark cycles, such as those experienced in shift work, can disrupt reproductive function and compromise fertility, especially in women. This research aimed to assess the effects of circadian disruption on female reproductive function and investigate the underlying neuroendocrine mechanisms. In female mice, exposure to a light-based shift work model led to a major desynchronization of the preovulatory LH surge, which persisted for several weeks. This disruption was associated with altered transmission of daily signals from the master circadian clock to kisspeptin neurons, which regulate LH secretion. Additionally, reproductive outcomes in mice were affected, though without any major impact on offspring development

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Paaske, Lauren K. "AVPV kisspeptin neurons mediate neuroprogesterone induction of the luteinizing hormone surge". Thesis, California State University, Long Beach, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1526942.

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Ovulation requires neural circuits in the brain to be sequentially exposed to estradiol and progesterone in the female rat. Estradiol-induced neuroprogesterone is essential for the luteinizing hormone (LH) surge and subsequently, ovulation to occur. The LH surge is regulated by gonadotropin-releasing hormone (GnRH) neurons in the diagonal band of Broca (DBB) which do not express progesterone receptors (PR), but are closely associated with anteroventral periventricular nucleus (AVPV) PR-expressing kisspeptin neurons. I tested the hypothesis that estradiol-induced neuroprogesterone activates AVPV kisspeptin neurons to trigger the LH surge. Inhibiting progesterone synthesis blocked estradiol induction of the LH surge that was rescued by subsequent treatment with either progesterone or DBB kisspeptin infusion. Estradiol treatment triggered a robust LH surge that was blocked by AVPV kisspeptin asODN infusion. These results support the hypothesis that neuroprogesterone induces kisspeptin release from AVPV neurons to activate DBB GnRH neurons and trigger the LH surge.

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Maze, Timothy D. "Development of the induced gonadotropin surge mechanism in the prepubertal heifer". Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2525.

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Thesis (Ph. D.)--West Virginia University, 2002.
Title from document title page. Document formatted into pages; contains viii, 71 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 61-70).

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Chuon, Timbora. "Src Kinase Signaling Pathway Mediates Neuroprogesterone Induction of the Luteinizing Hormone Surge". Thesis, California State University, Long Beach, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10839349.

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Ovulation is regulated by feedback mechanisms that include systems of astrocyte-neuronal interactions responsive to estradiol and progesterone in the rat. Estradiol induces progesterone receptors (PGRs) in rostral periventricular region of the third ventricle (RP3V) kisspeptin neurons, and positive feedback estradiol concentrations induce neuroprogesterone (neuroP) synthesis in hypothalamic astrocytes that signal to PGRs expressed in kisspeptin neurons to trigger the LH surge. I tested the hypothesis that neuroP-PGR signals through Src family kinase (Src) to trigger the LH surge. PGR and Src are co-expressed in RP3V neurons and their colocalization and immunopositive cells are upregulated with estradiol treatment. RP3V infusions of Src inhibitor (PP2) attenuated the LH surge in 50µg EB primed ovariectomized/adrenalectomized (ovx/adx) rats. In 2µg EB primed animals, infusions of Src activator and PGR triggered the LH surge. These results support my hypothesis that neuroprogesterone signals through RP3V PGR-Src complexes in kisspeptin neurons to induce the LH surge.

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Liu, Tang-Yu. "A Mathematical Model for the Luteinizing Hormone Surge in the Menstrual Cycle". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1471606050.

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Richter, Trevor Aubrey. "Investigation of the blockade of the estradiol-induced luteinizing hormone surge by progesterone". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620945.

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Pierson, Janice. "The influence of season on preovulatory events associated with estrus synchronization in dwarf goats raised in Quebec". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0033/MQ64430.pdf.

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Breckenridge, Charles B., Chad D. Foradori, Coder Pragati Sawhney, James W. Simpkins, Robert L. Sielken y Robert J. Handa. "Changes in Sensitivity to the Effects of Atrazine on the Luteinizing Hormone Surge in Female Sprague-Dawley Rats after Repeated Daily Doses: Correlation with Liver Enzyme Expression". WILEY, 2018. http://hdl.handle.net/10150/627193.

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BackgroundAtrazine suppression of the LH surge slowly develops over time and peaks after 4 days; sensitivity to atrazine decreases after 8 or 14 days of dosing. Adaptation of the LH response was correlated with increased phase I and phase II liver enzyme activity/expression. MethodsThe effect of atrazine on the LH surge was evaluated in female Sprague-Dawley rats administered 100 mg/kg/day atrazine by gavage for 1, 2, 3, or 4 consecutive days or 6.5, 50, or 100 mg/kg/day atrazine for 4, 8, or 14 days. ResultsNo statistically significant effects of atrazine were seen on peak plasma LH or LH area under the curve (AUC) after one, two, or three doses of 100 mg/kg/day. Four daily doses of 50 or 100 mg/kg atrazine significantly reduced peak LH and LH AUCs, whereas 6.5 mg/kg/day had no effect. After 8 or 14 days of treatment, statistically significantly reduced peak LH and LH AUC were observed in the 100 mg/kg/day dose group, but not in the 6.5 or 50 mg/kg/day dose groups, although significantly reduced LH was observed in one sample 9 hr after lights-on in the 50 mg/kg/day dose group on day 14. The number of days of treatment required to achieve a significant suppression of the LH surge is consistent with the repeat-dose pharmacokinetics of the chlorotriazines. ConclusionThe apparent adaptation to the effect of atrazine on the LH surge after 8 or 14 days may be related to the induction of phase I or, more likely, phase II metabolism observed in this study after 8 days, or to a decreased sensitivity of the hypothalamic-pituitary-adrenal axis or an homeostatic adaption of the effect of atrazine on the LH surge mechanism. Birth Defects Research 110:246-258, 2018. (c) 2017 The Authors. Birth Defects Research Published by Wiley Periodicals, Inc.

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Bahougne, Thibault. "Perturbation de la rythmicité circadienne : impact sur la fonction reproductive de souris femelles". Thesis, Strasbourg, 2020. http://www.theses.fr/2020STRAJ001.

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Chez les mammifères femelles, la fonction reproductive dépend à la fois d’une horloge biologique synchronisée par le cycle lumière/obscurité et par un équilibre entre le rétrocontrôle négatif et positif des œstrogènes, dont les concentrations varient en fonction de la maturation folliculaire. Chez les femmes, un nombre croissant d’études signalent un impact négatif des environnements chronodisruptifs, comme le travail posté / de nuit, sur la fertilité. Les objectifs de mon travail étaient d’étudier les effets d’un décalage de phase unique ou chronique sur les cycles reproducteurs de souris (C57BL/6J) femelles adultes. Dans ce but j’ai 1) mis au point un modèle de suivi longitudinal (sur plusieurs mois) de la sécrétion de LH le jour du proestrus sur des individus uniques ; 2) analysé les effets d’une avance ou d’un retard de phase unique (10h) sur les cycles estriens et l’occurrence du pic préovulatoire de LH ; 3) analysé les effets d’avance/retard de phases chroniques (jusqu’à 9 mois) sur les cycles estriens, le pic préovulatoire de LH et la fertilité ; 4) mis au point d’injection intra-cérébro-ventriculaire (ICV) de peptides associée au suivi individuel de LH afin de proposer des méthodes de resynchronisation du pic préovulatoire de LH chez des souris soumises à des déphasages. Mes travaux montrent qu’une avance ou un retard de phase unique perturbe peu le cycle reproducteur des souris femelles jeunes tandis qu’un décalage chronique altère fortement à la fois la régularité des cycles estriens, la sécrétion préovulatoire de LH et la fertilité. Ces données fondamentales démontrent un impact négatif de la perturbation chronique des cycles journaliers sur l'axe reproducteur des souris femelles. Une extrapolation de nos données fondamentales chez la femme, notamment dans un contexte de travail posté, est à l’heure actuelle prématurée. Cependant, au vu de nos résultats, une étude prospective chez la femme est indispensable
In female mammals, cycles in reproductive function depend on both a biological clock synchronized to the light/dark cycle, and a balance between the negative and positive feedbacks of estradiol which concentration varies during ovary maturation. In women, studies report that chronodisruptive environments, notably those experienced in shiftwork conditions, may impair fertility and gestational success. The objective of this study was to explore, in female mice, the effects of shifted light/dark cycles on both the robustness of the estrous cycles and the timing of the preovulatory luteinizing hormone (LH) surge, two hallmarks of mammalian reproductive health. When mice were exposed to a single 10 h-phase advance or 10 h-phase delay, the occurrence and timing of the LH surge and estrous cyclicity were recovered at the third estrous cycle. By contrast, when mice were exposed to a chronic shift (successive rotations of 10 h-phase advance for 3 days followed by 10 h-phase delay for 4 days), they exhibited a severely impaired reproductive activity. Most mice had no preovulatory LH surge already at the beginning of the chronic shift. Furthermore, the gestational success of mice exposed to a chronic shift was reduced since the number of pups was two times lower in shifted as compared to control mice. In conclusion, this study reports that female mice exposure to a single-phase shift has minor reproductive effects whereas exposure to chronically disrupted light/dark cycles markedly impairs the preovulatory LH surge occurrence, leading to reduced fertility

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"Effect of Maternal Age on Transcriptome of Granulosa Cells from Bovine Dominant Follicles". Thesis, 2014. http://hdl.handle.net/10388/ETD-2014-01-1364.

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Advanced maternal age has been shown to influence follicular and luteal dynamics in bovine ovary resulting in reduced fertility. The overall objective of the four studies presented in this thesis is to identify the maternal age-associated transcriptional changes in granulosa cells of the dominant follicles during follicle development. In the first study, mRNA expression levels of housekeeping genes were measured by real–time quantitative PCR (RT-qPCR) in granulosa cells of dominant follicles and FSH-stimulated follicles to select and validate suitable reference genes for relative gene expression analyses during maternal and follicular aging. Stability of six reference genes (GAPDH, ACTB, EIF2B2, UBE2D2, SF3A1 and RNF20) was analyzed using GeNorm, DeltaCT and NormFinder programs and comprehensive ranking order was determined based on these programs. Geometric mean of multiple genes (UBE2D2, EIF2B2, GAPDH and SF3A1) was more appropriate reference control than individual genes for the comparison of relative gene expression among dominant and FSH-stimulated follicles during maternal and/or follicular aging studies. In the second study, maternal age-associated changes in the transcriptome of granulosa cells recovered at the time of selection of the dominant follicle from aged (n=3) and young cows (n=3) were determined by EmbryoGENE bovine oligo-microarrays (EMBV3, Agilent Technology). The mRNA expression of five transcripts (CYP19A1, PCNA, GJA1, TPM2, and VNN1) was confirmed in a different set of granulosa cell samples by RT-qPCR to validate microarray data. A total of 169 genes/isoforms were differentially expressed (≥ 2-fold-change; P ≤ 0.05) in aged cows vs. young cows. These transcripts revealed inefficient 1) control of gonadotropins, and gonadotropin-induced changes in the cytoskeleton and extracellular matrix, 2) lipid metabolism and steroidogenesis 3) cell proliferation, cell cycle control and intercellular communication, and 4) higher oxidative stress responses in aged cows vs. young cows. In the third study, changes in the transcriptome of granulosa cells of the preovulatory follicle 24 h after LH treatment from aged (n= 3) and young (n=3) were determined. A total of 1340 genes were expressed differentially (≥ 2-fold change; P ≤ 0.05) in aged cows vs. young cows. The mRNA expression of five transcripts (RGS2, PTGS2, TNFAIP6, VNN1, NR5A2 and GADD45B) was confirmed in a different set of granulosa cell samples to validate microarray data. These transcripts were related to delayed 1) response to LH treatment 2) cellular differentiation and luteinization and 3) progesterone synthesis. Intra-follicle levels of progesterone were lower (P < 0.05) in aged cows compared to young and mid-aged cows. The fourth study compared the aged-associated changes in the transcriptome of granulosa cells during follicle development from the time of dominant follicle selection to preovulatory stage (24 h after LH). In comparison to young cows, aged cows expressed fewer differentially expressed genes/isoforms (1206 vs. 2260, respectively) at ≥ 2-fold-change (P ≤ 0.05) in the granulosa cells of the preovulatory (24 h after LH treatment) vs. the dominant follicle at selection. These transcripts in aged cows were related to late and inefficient 1) organization of cytoskeleton and cytoplasm, 2) differentiation, 3) lipid and cholesterol metabolism, 4) proliferation and 5) higher response to oxidative stress and free radical scavenging in the preovulatory follicles vs. the dominant follicle at selection. In conclusion, maternal age-alters the gene expression of granulosa cells of the dominant follicles during follicle development and results in a compromised follicular environment.

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Libros sobre el tema "Preovulatory luteinizing hormone surge"

M, Goldman Jerome y United States. Environmental Protection Agency, eds. Influence of the formamidine pesticide chlordimeform on ovulation in the female hamster: Dissociable shifts in the luteinizing hormone surge and oocyte release. [Washington, D.C.?: Environmental Protection Agency, 1993.

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Capítulos de libros sobre el tema "Preovulatory luteinizing hormone surge"

Karsch, Fred J., Suzanne M. Moenter y Alain Caraty. "The Preovulatory Surge of Gonadotropin Releasing Hormone". En Modes of Action of GnRH and GnRH Analogs, 241–55. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_16.

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"Reproductive Neuroendocrine Regulation in the Female: Toward a Neurochemical Mechanism for the Preovulatory Luteinizing Hormone Surge". En Reproductive and Developmental Toxicology, 171–228. CRC Press, 1998. http://dx.doi.org/10.1201/9781420002898-9.

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Owen, Corie M. y Laurinda A. Jaffe. "Luteinizing hormone-induced changes in the structure of mammalian preovulatory follicles". En Current Topics in Developmental Biology. Elsevier, 2024. http://dx.doi.org/10.1016/bs.ctdb.2024.10.011.

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Gangat, Naseema. "Benign Hematologic Disorders". En Mayo Clinic Internal Medicine Board Review, 399–414. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190464868.003.0037.

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The menstrual cycle is composed of the follicular (proliferative), periovulatory, and luteal (secretory) phases. At periovulation, the mature follicle triggers a surge in luteinizing hormone level, causing ovum release and stimulating the residual ovarian follicle to transform into a corpus luteum. Circulating estrogen and progestin levels increase. A thickened, enriched endometrium develops owing to progestin secretion from the corpus luteum. Without fertilization, the corpus luteum atrophies, estrogen and progestin levels decline, follicle-stimulating hormone release is stimulated, and the endometrium sloughs.

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Hedricks, Cynthia, Linda J. Piccinino y J. Richard Udry. "A First Attempt at Estimating Luteinizing Hormone Surge Onset Day at Midcycle". En Menstruation, Health, and Illness, 59–64. Taylor & Francis, 2019. http://dx.doi.org/10.4324/9781315793078-7.

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Lee-Chiong, Teofilo. "Sleep in Women". En Sleep Medicine: Essentials and Review, 445–60. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306590.003.0015.

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Abstract Sleep can be affected by changes in reproductive cycles across the lifespan of women. Levels of estrogen and progesterone vary throughout the reproductive years, with a monthly cyclic pattern associated with menstruation, increasing during pregnancy, returning to preconception levels after delivery, and declining during perimenopause and menopause. Compared with men, women generally have more subjective complaints of insufficient or nonrestorative sleep while reporting a greater need for sleep. The usual 28to 30-day menstrual cycle is divided into two phases, each lasting about 14 to 15 days. The initial follicular phase starts on the first day of menses. Estrogen is the predominant hormone during this phase. The second luteal phase begins at ovulation, with the peak of the surge in levels of luteinizing hormone brought about by rising levels of estrogen and progesterone. The subsequent menstruation is preceded by withdrawal of estrogen and progesterone. Mean daily body temperatures are lower by about 0.4°C during the follicular phase when compared with the luteal phase. Regular menstrual cycles start at menarche and end at menopause.

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Poletto, Karine Queiroz, Eduardo Camelo de Castro, Gabriella Reis de Barros Ribeiro y Thaiz Brandão Cosac. "Follicular waves in the human ovary". En Medicine: an exploration of the anatomy of the human body. Seven Editora, 2024. http://dx.doi.org/10.56238/sevened2024.005-004.

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Follicular waves can be defined as a synchronized growth of a group of antral follicles, among which one or more follicles will be selected for subsequent development and ovulation. These waves occur at regular intervals during the menstrual cycle. The synchronization of the wave beginning and the ovarian stimulation improves the outcomes of the IVF treatment. Follicular waves are a natural phenomenon, and they develop in association with increased concentration of follicle stimulating hormone levels. Studies indicate that the follicular recruitment event occurs only once during the cycle; however, recent studies suggest that the recruitment can occur more than once during the same cycle. Several studies have demonstrated groups of women with two follicular waves and others with up to three waves during the normal menstrual cycle. Follicles recruited during these waves have the potential to ovulate in the presence of an luteinizing hormone surge, providing women, especially the poor responders, a more efficient and less expensive treatment. The majority of studies agree that there is not just a single wave of follicular recruitment during a menstrual cycle and this involves the optimization of treatment of poor responders, expanding the window of action for oocyte retrieval and avoiding expensive treatments.

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Chandel, Shobhini, Saumya Das, Smriti Ojha y Manisha Pandey. "Hormonal Imbalances and Genetic Factors in Menstrual Cycle Irregularities". En Women's Health: A Comprehensive Guide to Common Health Issues in Women, 101–28. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815256291124010008.

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The menstrual cycle refers to the hormone-related, rhythmic, repeating processes in a woman's body that are accompanied by monthly bleeding. A woman's body goes through changes during her menstrual cycle that are intended to establish the perfect conditions for the start and continuation of her pregnancy. Basic biological processes encompassing the ovary, anterior pituitary, cerebellum, and endometrial make up the menstrual cycle. Environmental factors, including stress, intense exercise, eating disorders, and obesity, can easily disturb the menstrual cycle, even with all of its complexity. Genetic issues include fragile X permutations, X chromosomal abnormalities, and point mutations in the enzyme galactose-1-phosphate uridyltransferase (GALT) (galactosemia), which can potentially interfere with the menstrual cycle. The intricate surge and variations in a variety of distinct reproductive hormones control the menstrual cycle. Together, these hormones help a woman's body get ready for pregnancy. The hypothalamus and pituitary gland regulate six important hormones, and the hypothalamus also secretes GnRH. FSH and luteinizing hormone LH are both a result of pituitary production when GnRH is present in the body. Under the direction of FSH and LH, the ovaries release testosterone, progesterone, and estrogen, as well as other hormones. The development of menstruation function is influenced by the start of puberty (adolescence). Menarche, or the onset of the first period, often occurs between the ages of 11 and 14 years, following which the menstrual cycle becomes regular for 1 to 1.5 years. Adolescent girls frequently experience menstrual issues, with an average occurrence rate of about 50%. These issues include amenorrhea, dysmenorrhea, premenstrual syndrome, and irregular uterine bleeding. While the majority of problems are minor—such as variations in period duration and flow—on occasion, they may be sufficiently serious to require hospitalization, especially in the instance of extreme malfunctioning uterine bleeding.

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