References of "Parent, Anne-Simone"
     in
Bookmark and Share    
Full Text
See detailSexually dimorphic effect of gestational exposure to BPA on DNA methylation pattern in the rat placenta
FUDVOYE, Julie ULg; Dehan, Pierre ULg; Trooskens, Gheert et al

Conference (2014, October 27)

Detailed reference viewed: 13 (2 ULg)
Full Text
See detailA novel mutation of the luteinizing hormone/choionic gonadotrophin receptor gene leading to Leydig cell hypoplasia type I
Potorac, Iulia ULg; Rivero-Müller, Adolfo; Pintiaux, Axelle ULg et al

in Abstract book - 24th Meeting of the Belgian Endocrine Society (2014, October 18)

Detailed reference viewed: 16 (6 ULg)
Peer Reviewed
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.) (2014), (44), 63-72

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 ▲]

Detailed reference viewed: 16 (4 ULg)
Full Text
Peer Reviewed
See detailNormal minipuberty in a patient with DAX-1 mutation: additional evidence of a differential role for DAX-1 during development?
FUDVOYE, Julie ULg; BOURGUIGNON, Jean-Pierre ULg; PARENT, Anne-Simone ULg

Poster (2014, March)

Classically, mutations in the DAX-1 gene cause an adrenal hypoplasia congenita associated with adrenal insufficiency and hypogonadotrophic hypogonadism. However, mini-puberty onset seems to be normal in ... [more ▼]

Classically, mutations in the DAX-1 gene cause an adrenal hypoplasia congenita associated with adrenal insufficiency and hypogonadotrophic hypogonadism. However, mini-puberty onset seems to be normal in those patients suggesting a normal function of the pituitary-gonadal axis during the perinatal period. [less ▲]

Detailed reference viewed: 26 (0 ULg)
Full Text
Peer Reviewed
See detailLA PERTURBATION ENDOCRINIENNE : entre enjeux de recherche, enjeux de santé publique et enjeux de pratique quotidienne
FUDVOYE, Julie ULg; Franssen, Delphine ULg; Naveau, Elise et al

in Revue Médicale de Liège (2014)

Epidemiological and experimental data highlight the fetal and early postnatal life as critical periods for the effects of endocrine disrupting chemicals (EDCs), since exposure to EDCs during these periods ... [more ▼]

Epidemiological and experimental data highlight the fetal and early postnatal life as critical periods for the effects of endocrine disrupting chemicals (EDCs), since exposure to EDCs during these periods can predispose to disease later in life. EDCs’ effects include 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). They could also influence the development of the cerebral cortex. However, the demonstration of the involvement of a single EDC remains difficult in human since we are virtually exposed to a mixture of several ubiquitous EDCs which are variably persistent in the environment and the body and have lifelong consequences. Moreover, since their dose-response relationship can be non-monotonic, setting a threshold dose for EDCs effects has become meaningless. Pregnant women, newborns and young children appear to be mostly at risk. However, the role of the physician remains difficult and raises several questions: how can we formulate justified, applicable and updated recommendations that are not counterproductive or alarmist…in a society that has to take the necessary steps to regulate production and protect the population? [less ▲]

Detailed reference viewed: 4 (0 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 22 (2 ULg)
Full Text
Peer Reviewed
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)

Detailed reference viewed: 14 (1 ULg)
Full Text
Peer Reviewed
See detailDelayed puberty in a girl due to an inactivating mutation of the LH receptor
FUDVOYE, Julie ULg; PARENT, Anne-Simone ULg; Bourguignon, Jean-Pierre ULg

Poster (2012, March)

We report the case of a 46 XY patient with a disorder of sex differentiation (DSD) caused by an inactivating mutation of the LH receptor. Mutations of genes involved in hypothalamic-pituitary-gonadal ... [more ▼]

We report the case of a 46 XY patient with a disorder of sex differentiation (DSD) caused by an inactivating mutation of the LH receptor. Mutations of genes involved in hypothalamic-pituitary-gonadal function are rare but they provide an experience of nature for understanding the physiology and the pathophysiology of gonadotropins actions. There arise from correlation between the phenotypes and genotypes in those unique conditions. Management of this particular patient with no LH activity involves oestrogen replacement therapy to induce breast development together with a gonadectomy due to the risk of gonadoblastoma in streak gonads. [less ▲]

Detailed reference viewed: 5 (0 ULg)
Full Text
Peer Reviewed
See detailSynCAM1, a synaptic adhesion molecule, is expressed in astrocytes and contributes to erbB4 receptor-mediated control of
Sandau, Ursula; Mungenast, Ally; Alderman, Z et al

in Endocrinology (2011), 152

Detailed reference viewed: 6 (1 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 33 (9 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 29 (6 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 30 (2 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 110 (9 ULg)