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Book: Androgens in childhood

Forest, Maguelone G.

biologocial, physiological, clinical and therapeutic aspects ; 23 tables

(Pediatric and adolescent endocrinology ; 19)

1989

Author's details	vol. ed. Maguelone G. Forest
Series title	Pediatric and adolescent endocrinology ; 19
Collection
Keywords	Androgens ; Endocrine Diseases / in infancy & childhood ; Sex Differentiation Disorders ; Kind ; Androgene ; Störung
Subject	Perturbation ; Beeinträchtigung ; Störungen ; Männliche Sexualhormone ; Kindheit ; Kindesalter ; Kindschaft ; Kinder
Language	English
Size	VI, 281 S. : Ill., graph. Darst.
Publisher	Karger
Publishing place	Basel u.a.
Publishing country	Switzerland
Document type	Book
HBZ-ID	HT003465078
ISBN	3-8055-4850-8 ; 978-3-8055-4850-2
Database	Catalogue ZB MED Medicine, Health

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1990 A 1359	order for loan	Magazin

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Book ; Conference proceedings: Endocrinologie sexuelle de la période périnatale

Forest, Maguelone G.

International Symposium on Sexual Endocrinology of the Perinatal Period, Lyon, France, May 30 - 31, 1974 = Sexual endocrinology of the perinatal period

(Les colloques de l'Institut National de la Santé et de la Recherche Médicale ; 32)

1974

Title variant	Sexual endocrinology of the perinatal period
Institution	Institut National de la Santé et de la Recherche Médicale / Unité de Recherches Endocriniennes et Métaboliques chez l'Enfant
Event/congress	International Symposium on Sexual Endocrinology of the Perinatal Period (1974, Lyon)
Author's details	INSERM, Unité de Recherches Endocriniennes et Métaboliques chez l'Enfant.Publ. sous la responsabilité de Maguelone G. Forest
Series title	Les colloques de l'Institut National de la Santé et de la Recherche Médicale ; 32 INSERM Colloque
Collection	INSERM Colloque
Language	French ; English
Size	424 S. : Ill., graph. Darst.
Publishing place	Paris
Publishing country	France
Document type	Book ; Conference proceedings
Note	Beitr. teilw. engl., teilw. franz.
HBZ-ID	HT002430449
Database	Catalogue ZB MED Medicine, Health

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1975 A 1298	order for loan	Magazin

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Article: Recent advances in the diagnosis and management of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

Forest, Maguelone G

Human reproduction update

2004 Volume 10, Issue 6, Page(s) 469–485

Abstract: Congenital adrenal hyperplasias (CAH) are inherited defects of cortisol biosynthesis. More than 90% of CAH are caused by 21-hydroxylase deficiency (21-OHD), found in 1:10 000 to 1:15 000 live births. Females with 'classical' 21-OHD, being exposed to ... ...

Abstract	Congenital adrenal hyperplasias (CAH) are inherited defects of cortisol biosynthesis. More than 90% of CAH are caused by 21-hydroxylase deficiency (21-OHD), found in 1:10 000 to 1:15 000 live births. Females with 'classical' 21-OHD, being exposed to excess androgens prenatally, are born with virilized external genitalia. Potentially lethal adrenal insufficiency is characteristic of two-thirds to three-quarters of patients with the classical salt wasting (SW) form of 21-OHD. Non-SW 21-OHD may be diagnosed on genital ambiguity in affected females, and/or later on the occurrence of androgen excess in both sexes. Non-classical 21-OHD, detected in > or =1:100 of certain populations, may present as precocious pubarche in children or polycystic ovarian syndrome in young women. 21-OHD is caused by mutations in the CYP21 gene encoding the steroid 21-hydroxylase enzyme. More than 90% of these mutations result from intergenic recombination between CYP21 and the closely linked CYP21P pseudogene. The degree to which each mutation compromises enzymatic activity is strongly correlated with the clinical severity of the disorder. This close association between genotype and phenotype makes it possible to predict clinical outcome in affected subjects. The risk of SW and prenatal virilization can be estimated, and overtreatment can be avoided in mildly affected cases. Glucocorticoid and mineralocorticoid replacement therapies are the mainstays of treatment, but additional therapies are being developed. A first trimester prenatal diagnosis should be proposed in families in whom molecular studies have been performed previously. The state of heterozygotism can be predicted by hormonal testing and confirmed by molecular studies. Prenatal diagnosis by direct mutation detection in previously genotyped families permits prenatal treatment of affected females in order to avoid or minimize genital virilization. Neonatal screening by hormonal methods identifies affected children before SW crises develop, reducing mortality in this disorder.
MeSH term(s)	Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/epidemiology ; Adrenal Hyperplasia, Congenital/etiology ; Adrenal Hyperplasia, Congenital/therapy ; Body Height ; Dose-Response Relationship, Drug ; Female ; Fertility ; Genetic Counseling ; Glucocorticoids/therapeutic use ; Heterozygote ; Humans ; Incidence ; Infant, Newborn ; Mineralocorticoids/therapeutic use ; Mutation ; Neonatal Screening ; Obstetric Surgical Procedures/methods ; Pregnancy ; Prenatal Diagnosis/methods ; Steroid 21-Hydroxylase/genetics ; Treatment Outcome
Chemical Substances	Glucocorticoids ; Mineralocorticoids ; Steroid 21-Hydroxylase (EC 1.14.14.16)
Language	English
Publishing date	2004-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1286738-x
ISSN	1460-2369 ; 1355-4786
ISSN (online)	1460-2369
ISSN	1355-4786
DOI	10.1093/humupd/dmh047
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A case of 3beta-hydroxysteroid dehydrogenase type II (HSD3B2) deficiency picked up by neonatal screening for 21-hydroxylase deficiency: difficulties and delay in etiologic diagnosis.

Nordenström, Anna / Forest, Maguelone G / Wedell, Anna

Hormone research

2007 Volume 68, Issue 4, Page(s) 204–208

Abstract: Background: 3beta-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia ...

Abstract	Background: 3beta-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia in females. The clinical signs may be difficult to recognize, increasing the risk of a neonatal adrenal crisis. In addition, elevated 17alpha-hydroxyprogesterone and androstenedione levels due to peripheral HSD3B1 activity may lead to a delay of the correct diagnosis and even to misdiagnosis as CYP21 deficiency. Method: We report a patient who was detected on neonatal screening for 21-hydroxylase deficiency, in part because of cross-reactivity in the commonly used assay. Results: The diagnostic difficulties in this case were overcome by the use of more specific antibodies. Conclusion: This case emphasizes the importance of confirming the etiological diagnosis with molecular genetic analyses.
MeSH term(s)	3-Hydroxysteroid Dehydrogenases/genetics ; Adrenal Hyperplasia, Congenital/diagnosis ; Adrenal Hyperplasia, Congenital/etiology ; Adrenal Hyperplasia, Congenital/genetics ; Diagnosis, Differential ; Female ; Humans ; Infant, Newborn ; Neonatal Screening
Chemical Substances	3-Hydroxysteroid Dehydrogenases (EC 1.1.-)
Language	English
Publishing date	2007
Publishing country	Switzerland
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	124442-5
ISSN	1423-0046 ; 0301-0163
ISSN (online)	1423-0046
ISSN	0301-0163
DOI	10.1159/000102593
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Androgens in childhood

Forest, Maguelone G

biological, physiological, clinical, and therapeutic aspects

(Pediatric and adolescent endocrinology ; vol. 19)

1989

Author's details	volume editor, Maguelone G. Forest
Series title	Pediatric and adolescent endocrinology ; vol. 19
MeSH term(s)	Child ; Infant ; Androgens ; Disorders of Sex Development ; Endocrine System Diseases
Language	English
Size	vi, 281 p. :, ill.
Publisher	Karger
Publishing place	Basel ; New York
Document type	Book
Note	Includes index.
ISBN	9783805548502 ; 3805548508
Database	Catalogue of the US National Library of Medicine (NLM)

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Article: A Case of 3β-Hydroxysteroid Dehydrogenase Type II (HSD3B2) Deficiency Picked up by Neonatal Screening for 21-Hydroxylase Deficiency: Difficulties and Delay in Etiologic Diagnosis

Nordenström, Anna / Forest, Maguelone G. / Wedell, Anna

Hormone Research in Paediatrics

2007 Volume 68, Issue 4, Page(s) 204–208

Abstract: Background: 3β-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia in ... ...

Institution	Department of Pediatrics and PKU Laboratory, and Department of Molecular Medicine and Surgery, Karolinska University Hospital Huddinge and Solna, Karolinska Institutet, Stockholm, Sweden Department of Pediatric Endocrinology, Hôpital Debrousse, Lyon, France
Abstract	Background: 3β-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia in females. The clinical signs may be difficult to recognize, increasing the risk of a neonatal adrenal crisis. In addition, elevated 17α-hydroxyprogesterone and androstenedione levels due to peripheral HSD3B1 activity may lead to a delay of the correct diagnosis and even to misdiagnosis as CYP21 deficiency. Method: We report a patient who was detected on neonatal screening for 21-hydroxylase deficiency, in part because of cross-reactivity in the commonly used assay. Results: The diagnostic difficulties in this case were overcome by the use of more specific antibodies. Conclusion: This case emphasizes the importance of confirming the etiological diagnosis with molecular genetic analyses.
Keywords	3β-Hydroxysteroid dehydrogenase type II ; <italic>HSD3B2</italic> gene ; Neonatal screening, congenital adrenal hyperplasia ; Assay cross-reactivity
Language	English
Publishing date	2007-05-10
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Novel Insights from Clinical Practice
ZDB-ID	2537278-6
ISSN	1663-2826 ; 1663-2818
ISSN (online)	1663-2826
ISSN	1663-2818
DOI	10.1159/000102593
Database	Karger publisher's database

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Article: Follicular cells acquire sertoli cell characteristics after oocyte loss.

Guigon, Céline J / Coudouel, Noëlline / Mazaud-Guittot, Séverine / Forest, Maguelone G / Magre, Solange

Endocrinology

2005 Volume 146, Issue 7, Page(s) 2992–3004

Abstract: Although it has been suggested that in mammals the loss of female germ cells may induce the masculinization of the ovarian compartment, there has been as yet no conclusive demonstration. To directly address that question, the present study has been ... ...

Abstract	Although it has been suggested that in mammals the loss of female germ cells may induce the masculinization of the ovarian compartment, there has been as yet no conclusive demonstration. To directly address that question, the present study has been designed to determine the fate of follicular cells after oocyte loss. Using gamma-irradiation to selectively deplete oocytes in nongrowing follicles in female rats, we show that follicular cells in oocyte-depleted follicles survive, proliferate, and subsequently acquire morphological characteristics of Sertoli cells: elongated cytoplasm, basal location of the nucleus, and specific Sertoli cell junctions, the ectoplasmic specializations. These Sertoli-like cells express, however, the female-specific marker FOXL2 (Forkhead L2) but not the male sex-specific marker SOX-9 (Sry-type high-mobility-group box transcription factor-9) underlying the maintenance of molecular characteristics of granulosa cells. Before transdifferentiating into Sertoli-like cells, follicular cells of oocyte-depleted follicles initiate the expression of anti-Mullerian hormone and inhibin alpha-subunit that are typically synthesized by granulosa cells from the onset of follicular growth. Experimental modifications of the endocrine balance of the irradiated females show that there is a close relationship between plasma FSH levels and the occurrence of Sertoli-like cells. In addition to providing experimental evidence for the crucial role of the oocyte in granulosa cell phenotype maintenance, these results emphasize that the transdifferentiation of granulosa cells into Sertoli cells occurs in a multistep fashion, requiring the maturation of granulosa cells and depending on the endocrine milieu.
MeSH term(s)	Animals ; Anti-Mullerian Hormone ; Biomarkers/metabolism ; Cell Differentiation/physiology ; Cell Survival/physiology ; DNA-Binding Proteins/metabolism ; Female ; Follicle Stimulating Hormone/blood ; Gamma Rays ; Glycoproteins/metabolism ; Granulosa Cells/physiology ; Inhibins/metabolism ; Male ; Oocytes/cytology ; Oocytes/radiation effects ; Ovarian Follicle/cytology ; Ovarian Follicle/metabolism ; Ovarian Follicle/physiology ; Phenotype ; Rats ; Sertoli Cells/cytology ; Sertoli Cells/physiology ; Testicular Hormones/metabolism ; Transcription Factors/metabolism
Chemical Substances	Biomarkers ; DNA-Binding Proteins ; Glycoproteins ; Testicular Hormones ; Transcription Factors ; inhibin-alpha subunit ; Inhibins (57285-09-3) ; Anti-Mullerian Hormone (80497-65-0) ; Follicle Stimulating Hormone (9002-68-0)
Language	English
Publishing date	2005-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2005-0045
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Diethylstilbestrol inhibits the expression of the steroidogenic acute regulatory protein in mouse fetal testis.

Guyot, Romain / Odet, Fanny / Leduque, Patrick / Forest, Maguelone G / Le Magueresse-Battistoni, Brigitte

Molecular and cellular endocrinology

2004 Volume 220, Issue 1-2, Page(s) 67–75

Abstract: This study investigated the early deleterious effects of an in-utero exposure to diethylstilbestrol (DES) on mouse testicular development. To that purpose, pregnant mice were injected daily with up to 100 microg/kg DES from 10.5 to 17.5 days postcoitum ( ... ...

Abstract	This study investigated the early deleterious effects of an in-utero exposure to diethylstilbestrol (DES) on mouse testicular development. To that purpose, pregnant mice were injected daily with up to 100 microg/kg DES from 10.5 to 17.5 days postcoitum (dpc). At 18.5 dpc, testes were removed from fetuses for RNA (RT-PCR) and protein (Western blot, immunohistochemistry) analysis. Twenty-two genes were selected among which transcription factors, markers of differentiation of the different testicular cell lineages, steroidogenic enzymes and hormone receptors. The Steroidogenic Acute Regulatory (StAR) protein produced by the fetal Leydig cells was dramatically reduced in the DES-exposed testes. The P450c17 was the other gene modified following DES exposure. The alteration of these two genes is consistent with the decrease observed in the intratesticular testosterone levels, in the DES-exposed testes. Collectively, we demonstrated that DES did not alter testicular cell lineage specification but that it strongly inhibited the major function of the fetal Leydig cells.
MeSH term(s)	3-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Blotting, Western ; DNA-Binding Proteins/metabolism ; Diethylstilbestrol/pharmacology ; Female ; Fetus/drug effects ; Fetus/metabolism ; Gene Expression Regulation/drug effects ; Homeodomain Proteins ; Immunohistochemistry ; Male ; Mice ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Pregnancy ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, Cytoplasmic and Nuclear ; Steroidogenic Factor 1 ; Testis/anatomy & histology ; Testis/drug effects ; Testis/metabolism ; Testosterone/metabolism ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; Homeodomain Proteins ; Phosphoproteins ; RNA, Messenger ; Receptors, Cytoplasmic and Nuclear ; Steroidogenic Factor 1 ; Transcription Factors ; steroidogenic acute regulatory protein ; Testosterone (3XMK78S47O) ; Diethylstilbestrol (731DCA35BT) ; 3-Hydroxysteroid Dehydrogenases (EC 1.1.-)
Language	English
Publishing date	2004-05-31
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2004.03.008
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Zs.A 1127: Show issues

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Article: Unaltered development of the initial follicular waves and normal pubertal onset in female rats after neonatal deletion of the follicular reserve.

Guigon, Céline J / Mazaud, Séverine / Forest, Maguelone G / Brailly-Tabard, Sylvie / Coudouel, Noëlline / Magre, Solange

Endocrinology

2003 Volume 144, Issue 8, Page(s) 3651–3662

Abstract: In rats, the pool of primordial follicles is established within the first 3 d postnatally (dpn). Immediately after their differentiation, a subset of follicles begins to grow and constitutes the initial follicular waves. In this study we investigated the ...

Abstract	In rats, the pool of primordial follicles is established within the first 3 d postnatally (dpn). Immediately after their differentiation, a subset of follicles begins to grow and constitutes the initial follicular waves. In this study we investigated the development of these early growing follicles after deletion of the primordial follicle pool induced by 1.5 Gy gamma-irradiation at 5 dpn. Within only 24 h, i.e. at 6 dpn, 99% of the primordial follicles disappeared, whereas most of the growing follicles remained unaffected. The study of these surviving follicles throughout the immature period has shown that their subsequent growth proceeded normally, as assessed by proliferating cell nuclear antigen immunostaining and follicular counts. No modification in the process of follicular atresia, studied by terminal deoxynucleotidyltransferase-mediated deoxy-UTP-fluorescein nick end labeling and Southern blot of DNA fragmentation analysis, was observed. Complementary analysis, by either in situ hybridization for inhibin subunits, P450 aromatase, and LH receptor mRNAs or plasma dosages of 17beta-estradiol and inhibin B, further showed that follicular maturation was unaltered. In line with these observations, pubertal onset was normal, regarding both age and ovulation rate. Nevertheless, as a consequence of the nonrenewal of the growing pool, the follicular complement was practically exhausted at puberty, and 90% of the females evidenced sterility by 4 months. Altogether, our results demonstrate that the deletion of the primordial follicle pool has induced no modification in the growth pattern of the early growing follicles that develop as their counterparts in control ovaries. Within the immature period, the initial follicular waves ensure the ovarian functionality and thus play a key role in the initiation of reproductive life.
MeSH term(s)	Animals ; Animals, Newborn ; Aromatase/genetics ; Blotting, Southern ; Cell Count ; DNA Fragmentation ; Estradiol/blood ; Female ; Follicular Atresia ; Gamma Rays ; In Situ Hybridization ; In Situ Nick-End Labeling ; Infertility, Female/etiology ; Inhibins/blood ; Inhibins/genetics ; Oocytes ; Ovarian Follicle/chemistry ; Ovarian Follicle/growth & development ; Ovarian Follicle/radiation effects ; Proliferating Cell Nuclear Antigen/analysis ; RNA, Messenger/analysis ; Rats ; Rats, Sprague-Dawley ; Receptors, LH/genetics ; Sexual Maturation
Chemical Substances	Proliferating Cell Nuclear Antigen ; RNA, Messenger ; Receptors, LH ; inhibin B ; Estradiol (4TI98Z838E) ; Inhibins (57285-09-3) ; Aromatase (EC 1.14.14.1)
Language	English
Publishing date	2003-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2003-0072
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Role of Androgens in Fetal and Pubertal Development

Forest, Maguelone G.

Hormone Research - From Developmental Endocrinology to Clinical Research

1983 Volume 18, Issue 1-3, Page(s) 69–83

Abstract: ... on specific organs during a critical phase of morphogenesis (e.g. sexual differentiation of external genitalia), or ...

Abstract	During fetal development, androgens exert long-term effects which are either organizational on specific organs during a critical phase of morphogenesis (e.g. sexual differentiation of external genitalia), or programming neural functions or enzyme activities expressed later in life. At all stages of development, which extends from fetal and neonatal stages to pubertal accomplishment, androgens also have activational effects that are immediate, multiple, reversible and dose dependent. Both types of actions are intricate during human development. This review will focus (1) on the intricate morphological and activational roles of androgens on sexual differentiation and pubertal development of the genital tract, external genitalia and mammary glands, and (2) on the organizational effects of androgens on four central nervous system functions: pituitary regulation of liver metabolism, gonadotropin secretions, sex dimorphic behavioral patterns, and ‘sexualization of the brain’. If the molecular basis of the immediate androgenic action is known, depending of androgen receptor’s availability and affinity, little is known of the way androgens exert their influence on either so various morphological processes or neuroendocrine imprinting.
Keywords	Androgen ; Sex differentiation ; Fetal life ; Puberty ; Liver metabolism ; Gonadotropin secretions ; Behavioral patterns ; Central nervous system
Language	English
Publisher	S. Karger AG
Publishing place	Basel
Publishing country	Switzerland
Document type	Article ; Online
ZDB-ID	124442-5
ISSN	1423-0046 ; 0301-0163 ; 0301-0163
ISSN (online)	1423-0046
ISSN	0301-0163
DOI	10.1159/000179780
Database	Karger publisher's database

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