References of "Parent, Anne-Simone"
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See detailPubertal timing after neonatal diethylstilbestrol exposure in female rats: Neuroendocrine vs peripheral effects and additive role of prenatal food restriction.
Franssen, Delphine ULg; Ioannou, Yiannis S.; Alvarez-Real, Alexandra et al

in Reproductive toxicology (Elmsford, N.Y.) (2013)

We studied the effects of neonatal exposure to diethylstilbestrol (DES) on pubertal timing in female rats. We examined associated neuroendocrine changes and effects of prenatal food restriction. Age at ... [more ▼]

We studied the effects of neonatal exposure to diethylstilbestrol (DES) on pubertal timing in female rats. We examined associated neuroendocrine changes and effects of prenatal food restriction. Age at vaginal opening was advanced after exposure to 10mug/kg/d of DES and delayed after 1mug/kg/d (subcutaneous injections). Using this lower dose, pulsatile GnRH secretion was slower at 25 days of age. Both doses reduced KiSS1 mRNA levels at 15 days of age. Using functional Kisspeptin promoter assay, 1 or 10muM DES reduced or increased KISS1 transcription, respectively. Leptin stimulatory effect on GnRH secretion in vitro (15 days of age) was reduced after prenatal food restriction and neonatal DES exposure (higher dose), both effects being cumulative. Thus, alterations in pubertal timing by DES neonatally are not unequivocally toward precocity, the level of exposure being critical. We provide evidence of neuroendocrine disruption and interaction with prenatal food availability. [less ▲]

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See detailL'hyperthyroidie neonatale: clinique et prise en charge therapeutique.
Petignot, S.; NYAMUGABO MUNYERE NKANA, Kindja ULg; Socin, H. Valdes et al

in Revue medicale de Liege (2013), 68(10), 531-6

Neonatal hyperthyroidism is a rare pathology, most often the consequence of Graves' disease in the mother. Around 0.2% of pregnant women have Graves disease and 1 to 2% of newborns of mother with Graves ... [more ▼]

Neonatal hyperthyroidism is a rare pathology, most often the consequence of Graves' disease in the mother. Around 0.2% of pregnant women have Graves disease and 1 to 2% of newborns of mother with Graves' disease. This article will describe the case of 4 newborns who have been diagnosed and treated in CHU-NDB between 2007 and 2011. The second part will focus on the new recommendations about the management of these young patients from foetal period to birth. [less ▲]

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See detailDepletion of the p43 Mitochondrial T3 Receptor Increases Sertoli Cell Proliferation in Mice
Fumel, Betty; Roy, Stéphanie; Fourchecourt, Sophie et al

in PLoS ONE (2013)

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See detailEarly developmental actions of endocrine disruptors on the hypothalamus, hippocampus, and cerebral cortex.
Parent, Anne-Simone ULg; Naveau, Elise; GERARD, Arlette ULg et al

in Journal of Toxicology and Environmental Health. Part B, Critical Reviews (2011), 14(5-7), 328-45

Sex steroids and thyroid hormones play a key role in the development of the central nervous system. The critical role of these hormonal systems may explain the sensitivity of the hypothalamus, the ... [more ▼]

Sex steroids and thyroid hormones play a key role in the development of the central nervous system. The critical role of these hormonal systems may explain the sensitivity of the hypothalamus, the cerebral cortex, and the hippocampus to endocrine-disrupting chemicals (EDC). This review examines the evidence for endocrine disruption of glial-neuronal functions in the hypothalamus, hippocampus, and cerebral cortex. Focus was placed on two well-studied EDC, the insecticide dichlorodiphenyltrichloroethane (DDT) and polychlorinated biphenyls (PCB). DDT is involved in neuroendocrine disruption of the reproductive axis, whereas polychlorinated biphenyls (PCB) interact with both the thyroid hormone- and sex steroid-dependent systems and disturb the neuroendocrine control of reproduction and development of hippocampus and cortex. These results highlight the impact of EDC on the developing nervous system and the need for more research in this area. [less ▲]

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See detailNeuroendocrine disruption of pubertal timing and interactions between homeostasis
Bourguignon, Jean-Pierre ULg; rasier, Gregory; Lebrethon, Marie-Christine ULg et al

in Molecular & Cellular Endocrinology (2010), 324(1-2), 110-120

The involvement of environmental factors such as endocrine disrupting chemicals (EDCs) in the timing of onset of puberty is suggested by recent changes in age at onset of puberty and pattern of ... [more ▼]

The involvement of environmental factors such as endocrine disrupting chemicals (EDCs) in the timing of onset of puberty is suggested by recent changes in age at onset of puberty and pattern of distribution that are variable among countries, as well as new forms of sexual precocity after migration. However, the evidence of association between early or late pubertal timing and exposure to EDCs is weak in humans, possibly due to heterogeneity of effects likely involving mixtures and incapacity to assess fetal or neonatal exposure retrospectively. The neuroendocrine system which is crucial for physiological onset of puberty is targeted by EDCs. These compounds also act directly in the gonads and peripheral sex-steroid sensitive tissues. Feedbacks add to the complexity of regulation so that changes in pubertal timing caused by EDCs can involve both central and peripheral mechanisms. In experimental conditions, several neuroendocrine endpoints are affected by EDCs though only few studies including from our laboratory aimed at EDC involvement in the pathophysiology of early sexual maturation. Recent observations support the concept that EDC cause disturbed energy balance and account for the obesity epidemic. Several aspects are linking this system and the reproductive axis: coexisting neuroendocrine and peripheral effects, dependency on fetal/neonatal programming and the many factors cross-linking the two systems, for instance leptin, adiponectin, Agouti Related Peptide (AgRP). This opens perspectives for future research and, hopefully, measures preventing the disturbances of homeostasis caused by EDCs. [less ▲]

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See detailEarly homeostatic disturbances of human growth and maturation by endocrine disrupters
Bourguignon, Jean-Pierre ULg; Parent, Anne-Simone ULg

in Current Opinion in Pediatrics (2010), 22(4), 470-477

We attempt to delineate and integrate aspects of growth and development that could be affected by endocrine disrupters [endocrine-disrupting compounds (EDC)], an increasing public health concern. RECENT ... [more ▼]

We attempt to delineate and integrate aspects of growth and development that could be affected by endocrine disrupters [endocrine-disrupting compounds (EDC)], an increasing public health concern. RECENT FINDINGS: Epidemiological and experimental data substantiate that fetal and early postnatal life are critical periods of exposure to endocrine disrupters, with possible transgenerational effects. The EDC effects include several disorders of the reproductive system throughout life (abnormalities of sexual differentiation, infertility or subfertility and some neoplasia) and disorders of energy balance (obesity and metabolic syndrome). The mechanisms are consistent with the concept of 'developmental origin of adult disease'. They could involve cross-talk between the factors controlling reproduction and those controlling energy balance, both in the hypothalamus and peripherally. SUMMARY: Due to ubiquity of endocrine disrupters and lifelong stakes of early exposure, individual families should be provided by pediatricians with recommendations following the precautionary principle, that is prevention or attenuation of conditions possibly detrimental to health before the evidence of such adverse effects is complete and undisputable. [less ▲]

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See detailComment j'EXPLORE ... un hypogonadisme hypogonadotrope congenital isole
Valdes-Socin, H.; Debray, François-Guillaume ULg; Parent, Anne-Simone ULg et al

in Revue Médicale de Liège (2010), 65(11), 634-41

Congenital Isolated hypogonadotropic hypogonadism (CIHH) is caused by an inherited mechanism of impairment of the pituitary-gonadal axis, interfering with gonads' control. Currently, different forms of ... [more ▼]

Congenital Isolated hypogonadotropic hypogonadism (CIHH) is caused by an inherited mechanism of impairment of the pituitary-gonadal axis, interfering with gonads' control. Currently, different forms of HHCI with (Kallmann syndrome or KS) or without anosmia-hyposmia are known. There are six forms of KS already described but in several cases no genetic mutation is found. The genetic anomalies already described are: KAL1 (locus Xp23) coding for anosmine-1, KAL-2 or FGFRI (8p11. locus 2 - p11.1) coding for Fibroblast Growth Factor Receptor 1 (FGFR1), KAL4 or PROk2 (locus 3p21.1) and KAL3 or ProKR2 (locus 20p13) coding respectively for the Prokinecitin-2 and its receptor, KAL5 or CHD7 (locus_8q12.1) coding for a chromodomain helicase DNA-binding protein-7 gene (CHD7) and lastly KAL6 or FGF8 (10Q 24 loci) coding for Fibroblast Growth Factor 8. The other genetic anomalies without anosmia are less frequent. These are associated either with Gnrhl gene (8p2-11. 2), GnRHR (4q21.2), GPR54 (19p13),TAC3R or neurokinine receptor 3 (4 q 25), LH (19q13.32) or FSH (11p13). The isolated congenital hypogonadotrophic hypogonadism phenotype is variable depending on gender, the importance of the deficit, and ultimately, according to a specific regulatory mechanism of the axis, affected by an inherited genetic anomaly. In this review, we describe the essential aspects of the different phenotypes and genotypes of HHCI, in order to assess clinicians an early disease's diagnosis and management. [less ▲]

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See detailOxytocin Facilitates Female Sexual Maturation through a Glia-to-Neuron Signaling Pathway
Parent, Anne-Simone ULg; Rasier, Grégory ULg; Matagne, V. et al

in Endocrinology (2008), 149(3), 1358-65

It has been earlier proposed that oxytocin could play a facilitatory role in the preovulatory LH surge in both rats and humans. We here provide evidence that oxytocin also facilitates sexual maturation in ... [more ▼]

It has been earlier proposed that oxytocin could play a facilitatory role in the preovulatory LH surge in both rats and humans. We here provide evidence that oxytocin also facilitates sexual maturation in female rats. The administration of an oxytocin antagonist for 6 d to immature female rats decreased GnRH pulse frequency ex vivo and delayed the age at vaginal opening and first estrus. The in vitro reduction in GnRH pulse frequency required chronic blockade of oxytocin receptors, because it was not acutely observed after a single injection of the antagonist. Hypothalamic explants exposed to the antagonist in vitro showed a reduced GnRH pulse frequency and failed to respond to oxytocin with GnRH release. Prostaglandin E(2) (PGE(2)) mimicked the stimulatory effect of oxytocin on GnRH pulse frequency, and inhibition of PG synthesis blocked the effect of oxytocin, suggesting that oxytocin accelerates pulsatile GnRH release via PGE(2). The source of PGE(2) appears to be astrocytes, because oxytocin stimulates PGE(2) release from cultured hypothalamic astrocytes. Moreover, astrocytes express oxytocin receptors, whereas GnRH neurons do not. These results suggest that oxytocin facilitates female sexual development and that this effect is mediated by a mechanism involving glial production of PGE(2). [less ▲]

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See detailMechanisms of Interaction of Endocrine-Disrupting Chemicals with Glutamate-Evoked Secretion of Gonadotropin-Releasing Hormone
Rasier, Gregory; Parent, Anne-Simone ULg; Gerard, Arlette ULg et al

in Toxicological Sciences (2008), 102(1), 33-41

In previous studies, we detected a dichlorodiphenyltrichloroethane (DDT) derivative in the serum of children with sexual precocity after migration from developing countries. Recently, we reported that DDT ... [more ▼]

In previous studies, we detected a dichlorodiphenyltrichloroethane (DDT) derivative in the serum of children with sexual precocity after migration from developing countries. Recently, we reported that DDT stimulated pulsatile gonadotropin-releasing hormone (GnRH) secretion and sexual maturation in the female rat. The aim of this study was to delineate the mechanisms of interaction of endocrine-disrupting chemicals including DDT with GnRH secretion evoked by glutamate in vitro. Using hypothalamic explants obtained from 15-day-old female rats, estradiol (E2) and DDT caused a concentration-related increase in glutamate-evoked GnRH release while p,p'-dichlorodiphenyldichloroethene and methoxychlor had no effect. The effective DDT concentrations in vitro were consistent with the serum concentrations measured in vivo 5 days after exposure of immature rats to 10 mg/kg/day of o,p'-DDT. Bisphenol A induced some stimulatory effect, whereas no change was observed with 4-nonylphenol. The o,p'-DDT effects in vitro were prevented partially by a selective antagonist of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtype of glutamate receptors. A complete prevention of o,p'-DDT effects was caused by an estrogen receptor (ER) antagonist as well as an aryl hydrocarbon receptor (AHR) antagonist and inhibitors of protein kinases A and C and mitogen-activated kinases. While an intermittent incubation with E2 caused no change in amplification of the glutamate-evoked GnRH release for 4 h, continuous incubation with E2 or o,p'-DDT caused an increase of this amplification after 3.5 h of incubation. In summary, DDT amplifies the glutamate-evoked GnRH secretion in vitro through rapid and slow effects involving ER, AHR, and AMPA receptor mediation. [less ▲]

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See detailGene expression profiling of hypothalamic hamartomas: a search for genes associated with central precocious puberty
Parent, Anne-Simone ULg; Matagne, Valérie; Westphal, Manfred et al

in Hormone Research (2008), 69

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See detailEarly maturation of gonadotropin-releasing hormone secretion and sexual precocity after exposure of infant female rats to estradiol or dichlorodiphenyltrichloroethane
Rasier, Gregory; Parent, Anne-Simone ULg; Gerard, Arlette ULg et al

in Biology of Reproduction (2007), 77(4), 734-742

An increase in the frequency of pulsatile gonadotropin-releasing hormone (GnRH) secretion in vitro and a reduction in LH response to GnRH in vivo characterize hypothalamic-pituitary maturation before ... [more ▼]

An increase in the frequency of pulsatile gonadotropin-releasing hormone (GnRH) secretion in vitro and a reduction in LH response to GnRH in vivo characterize hypothalamic-pituitary maturation before puberty in the female rat. In girls migrating for international adoption, sexual precocity is frequent and could implicate former exposure to the insecticide dichlorodiphenyltrichloroethane (DDT), since a long-lasting DDT derivative has been detected in the serum of such children. We aimed at studying the effects of early transient exposure to estradiol (E 2) or DDT in vitro and in vivo in the infantile female rat. Using a static incubation system of hypothalamic explants from 15-day-old female rats, a concentration- and time-dependent reduction in GnRH interpulse interval (IPI) was seen during incubation with E 2 and DDT isomers. These effects were prevented by antagonists of alpha-amino-3-hydroxy-5-methyl-isoxazole-4 propionic acid (AMPA)/kainate receptors and estrogen receptor. Also, o,p '-DDT effects were prevented by an antagonist of the aryl hydrocarbon orphan dioxin receptor (AHR). After subcutaneous injections of E, or o,p '-DDT between Postnatal Days (PNDs) 6 and 10, a decreased GnRH IPI was observed on PND 15 as an ex vivo effect. After DDT administration, serum LH levels in response to GnRH were not different from controls on PIND 15, whereas they tended to be lower on PND 22. Subsequently, early vaginal opening (VO) and first estrus were observed together with a premature age-related decrease in LH response to GnRH. After prolonged exposure to E 2 between PNDs 6 and 40, VO occurred at an earlier age, but first estrus was delayed. We conclude that a transient exposure to E 2 or o,p '-DDT in early postnatal life is followed by early maturation of pulsatile GnRH secretion and, subsequently, early developmental reduction of LH response to GnRH that are possible mechanisms of the subsequent sexual precocity. The early maturation of pulsatile GnRH secretion could involve effects mediated through estrogen receptor and/or AHR as well as AMPA/kainate subtype of glutamate receptors. [less ▲]

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See detailEffects of in vivo and in vitro administration of ghrelin, leptin and neuropeptide mediators on pulsatile gonadotrophin-releasing hormone secretion from male rat hypothalamus before and after puberty
Lebrethon, Marie-Christine; Aganina, Anastasia; Fournier, Michael et al

in Journal of Neuroendocrinology (2007), 19(3), 181-188

The present study aimed to investigate the effects of leptin and ghrelin on pulsatile pulsatile gonadotrophin-releasing hormone (GnRH) secretion in vitro with emphasis on neuropeptide mediators and ... [more ▼]

The present study aimed to investigate the effects of leptin and ghrelin on pulsatile pulsatile gonadotrophin-releasing hormone (GnRH) secretion in vitro with emphasis on neuropeptide mediators and changes between prepuberty (15 days) and sexual maturity (50 days) in the male rat. When hypothalamic explants were studied 90 min after an intraperitoneal injection of leptin, ghrelin or agouti-related protein (AgRP) at 15 days, the GnRH interpulse interval (IPI) was significantly increased by ghrelin and AgRP and decreased by leptin. At 50 days, an increase in GnRH IPI was also caused by ghrelin and AgRP. When the peptides were directly incubated with the explants, the effects of leptin and AgRP in vitro were consistent with those seen after in vivo administration. By contrast, ghrelin resulted in a reduction of GnRH IPI and this was observed at 15 days only. To delineate the neuropeptide mediators of leptin and the effects of ghrelin in the hypothalamus, various hypothalamic neuropeptides and antagonists were used in vitro. At 15 days, the GnRH IPI was significantly decreased after incubation with cocaine and amphetamine-regulated transcript (CART), alpha-melanocyte-stimulating hormone, corticotrophin-releasing factor (CRF) and neuropeptide Y (NPY). The reduction of GnRH IPI caused by leptin was partially prevented by either an anti-CART antiserum or SHU 9119, a melanocortin MC3/MC4 receptor antagonist or a CRF receptor antagonist. The NPY-Y5 receptor antagonist did not influence the effects of leptin whereas that antagonist totally prevented the decrease in GnRH IPI caused by ghrelin. The ghrelin-induced reduction of GnRH IPI was partially prevented by SHU 9119. When used alone, SHU 9119 or a CRF-receptor antagonist resulted in increased GnRH IPI at 50 days while they had no effects at 15 days. The NPY-Y5 receptor antagonist resulted in increased GnRH IPI at 15 and 50 days. In conclusion, leptin and ghrelin show opposing effects on pulsatile GnRH secretion after administration in vivo whereas they both have stimulatory effects in vitro. Such effects involve consistently the anorectic peptides CART and CRF for leptin that are mainly active at 15 days. The melanocortigenic system appears to mediate the effects of both leptin and ghrelin. The effects of ghrelin also involve NPY receptors and operate effectively before and at sexual maturity. [less ▲]

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See detailRégulation et dérégulation de l'âge pubertaire : populations à risque ?
Parent, Anne-Simone ULg; Domine, Françoise ULg; Charlier, Corinne ULg et al

in Revue Médicale de Liège (2007), 62

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See detailA contactin-receptor-like protein tyrosine phosphatase beta complex mediates adhesive communication between astroglial cells and gonadotropin-releasing hormone neurons
Parent, Anne-Simone ULg; Mungenast, Alison; Lomniczi, Alejandro et al

in Journal of Neuroendocrinology (2007), 19

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See detailAssessment and mechanism of variations in pubertal timing in internationally adopted children: a developmental hypothesis
Domine, Françoise ULg; Parent, Anne-Simone ULg; Rasier, Gregory et al

in European Journal of Endocrinology (2006), 155(Suppl. 1), 17-25

During the past decades, children migrating for international adoption have increased in number, creating an original condition of dramatic environmental change during development. In several countries ... [more ▼]

During the past decades, children migrating for international adoption have increased in number, creating an original condition of dramatic environmental change during development. In several countries, cohorts of these subjects have been shown to experience a global advancement in age at the onset of puberty, and sexual precocity is seen more frequently than in other conditions. Such early or precocious development has been assessed in relatively small cohorts or individual patients using well-defined physical indicators in comparison with updated references in the foster country. Family and adolescent evaluation of pubertal timing could allow for the study of large series of internationally adopted subjects. Also, this type of assessment integrates the physical changes of puberty with the adolescent changes in psychological and social functioning. The pathophysiological mechanisms leading to advancement of puberty in migrating children are still unclear and possibly involve several factors. In the present paper, we hypothesize that the sexual precocity in children migrating for international adoption could represent a developmentally programmed disorder resulting from cumulative anomalies in early remodeling of the central nervous system by communicational, social, nutritional, and hormonal inputs. There is some evidence that the deviations in those inputs can result in altered brain structure, particularly in the limbic system. We discuss the possible association with further disorders of developmental functions, such as cognitive, psychosocial, and sexual maturation. Along this hypothesis, some forms of idiopathic sexual precocity could result from dysfunction of one or several of the environmental programming factors, while other forms may involve predominantly genetic or familial factors. [less ▲]

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See detailFemale sexual maturation and reproduction after prepubertal exposure to estrogens and endocrine disrupting chemicals: A review of rodent and human data
Rasier, Gregory; Toppari, Jorma; Parent, Anne-Simone ULg et al

in Molecular & Cellular Endocrinology (2006), 254-255

Natural hormones and some synthetic chemicals spread into our surrounding environment share the capacity to interact with hormone action and metabolism. Exposure to such compounds can cause a variety of ... [more ▼]

Natural hormones and some synthetic chemicals spread into our surrounding environment share the capacity to interact with hormone action and metabolism. Exposure to such compounds can cause a variety of developmental and reproductive detrimental abnormalities in wildlife species and, potentially, in human. Many experimental and epidemiological data have reported that exposure of the developing fetus or neonate to environmentally relevant concentrations of some among these endocrine disrupters induces morphological, biochemical and/or physiological disorders in brain and reproductive organs, by interfering with the hormone actions. The impact of such exposures on the hypothalamic-pituitary-gonadal axis and subsequent sexual maturation is the subject of the present review. We will highlight epidemiological human studies and the effects of early exposure during gestational, perinatal or postnatal life in female rodents. (c) 2006 Elsevier Ireland Ltd. All rights reserved. [less ▲]

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