Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone

Autores
Recabarren, S. E.; Recabarren, Mónica; Sandoval, D.; Carrasco, A.; Padmanabhan, Vasantha; Rey, Rodolfo Alberto; Richter, Hans; Perez Marin, C. C.; Sir Petermann, Teresa; Rojas Garcia, P.P.
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The male gonadal tissue can be a sensitive target to the reprogramming effects of testosterone (T) during prenatal development. We have demonstrated that male lambs born to dams receiving T during pregnancyda model system to the polycystic ovary syndrome (PCOS)d show a decreased number of germ cells early in life, and when adult, a reduced amount of sperm and ejaculate volume. These findings are a key to put attention to the male offspring of women bearing PCOS, as they are exposed to increased levels of androgen during pregnancy which can reprogram their reproductive outcome. A possible origin of these defects can be a disruption in the expression of the anti-Müllerian hormone (AMH), due to its critical role in gonadal function at many postnatal stages. Therefore, we addressed the impact of prenatal T excess on the expression of AMH and factors related to its expression like AP2, SOX9, FSHR, and AR in the testicular tissue through real-time PCR during the peripubertal age. We also analyzed the testicular morphology and quantified the number of Sertoli cells and germ cells to evaluate any further defect in the testicle. Experiments were performed in rams at 24 wk of age, hence, prior puberty. The experimental animals (T-males) consisted of rams born to mothers receiving 30 mg testosterone twice a wk from Day 30 to 90 of pregnancy and then increased to 40 mg until Day 120 of pregnancy. The control males (C-males) were born to mothers receiving the vehicle of the hormone. We found a significant increase in the expression of the mRNA of AMH and SOX9, but not of the AP2, FHSR nor AR, in the T-males. Moreover, T-males showed a dramatic decrease in the number of germ cells, together with a decrease in the weight of their testicles. The findings of the present study show that before puberty, T-males are manifesting clear signs of disruption in the gonadal functions probably due to an alteration in the expression pattern of the AMH gene. The precise way by which T reprograms the expression of AMH gene remains to be established.
Fil: Recabarren, S. E.. Universidad de Concepción; Chile
Fil: Recabarren, Mónica. Universidad de Concepción; Chile
Fil: Sandoval, D.. Universidad de Concepción; Chile
Fil: Carrasco, A.. Universidad de Concepción; Chile
Fil: Padmanabhan, Vasantha. University of Michigan; Estados Unidos
Fil: Rey, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas ; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Richter, Hans. Universidad Austral de Chile; Chile
Fil: Perez Marin, C. C.. Universidad de Córdoba; España
Fil: Sir Petermann, Teresa. Universidad de Chile; Chile
Fil: Rojas Garcia, P.P.. Universidad de Concepción; Chile
Materia
Amh
Developmental Programming
Germ Cells
Pcos
Sertoli Cells
Testicle
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/51198
Acceder
id CONICETDig_35bcced8177d834cbf264e1755355cc7
oai_identifier_str oai:ri.conicet.gov.ar:11336/51198
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosteroneRecabarren, S. E.Recabarren, MónicaSandoval, D.Carrasco, A.Padmanabhan, VasanthaRey, Rodolfo AlbertoRichter, HansPerez Marin, C. C.Sir Petermann, TeresaRojas Garcia, P.P.AmhDevelopmental ProgrammingGerm CellsPcosSertoli CellsTesticlehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The male gonadal tissue can be a sensitive target to the reprogramming effects of testosterone (T) during prenatal development. We have demonstrated that male lambs born to dams receiving T during pregnancyda model system to the polycystic ovary syndrome (PCOS)d show a decreased number of germ cells early in life, and when adult, a reduced amount of sperm and ejaculate volume. These findings are a key to put attention to the male offspring of women bearing PCOS, as they are exposed to increased levels of androgen during pregnancy which can reprogram their reproductive outcome. A possible origin of these defects can be a disruption in the expression of the anti-Müllerian hormone (AMH), due to its critical role in gonadal function at many postnatal stages. Therefore, we addressed the impact of prenatal T excess on the expression of AMH and factors related to its expression like AP2, SOX9, FSHR, and AR in the testicular tissue through real-time PCR during the peripubertal age. We also analyzed the testicular morphology and quantified the number of Sertoli cells and germ cells to evaluate any further defect in the testicle. Experiments were performed in rams at 24 wk of age, hence, prior puberty. The experimental animals (T-males) consisted of rams born to mothers receiving 30 mg testosterone twice a wk from Day 30 to 90 of pregnancy and then increased to 40 mg until Day 120 of pregnancy. The control males (C-males) were born to mothers receiving the vehicle of the hormone. We found a significant increase in the expression of the mRNA of AMH and SOX9, but not of the AP2, FHSR nor AR, in the T-males. Moreover, T-males showed a dramatic decrease in the number of germ cells, together with a decrease in the weight of their testicles. The findings of the present study show that before puberty, T-males are manifesting clear signs of disruption in the gonadal functions probably due to an alteration in the expression pattern of the AMH gene. The precise way by which T reprograms the expression of AMH gene remains to be established.Fil: Recabarren, S. E.. Universidad de Concepción; ChileFil: Recabarren, Mónica. Universidad de Concepción; ChileFil: Sandoval, D.. Universidad de Concepción; ChileFil: Carrasco, A.. Universidad de Concepción; ChileFil: Padmanabhan, Vasantha. University of Michigan; Estados UnidosFil: Rey, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas ; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Richter, Hans. Universidad Austral de Chile; ChileFil: Perez Marin, C. C.. Universidad de Córdoba; EspañaFil: Sir Petermann, Teresa. Universidad de Chile; ChileFil: Rojas Garcia, P.P.. Universidad de Concepción; ChileElsevier Science Inc2017-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/51198Recabarren, S. E.; Recabarren, Mónica; Sandoval, D.; Carrasco, A.; Padmanabhan, Vasantha; et al.; Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone; Elsevier Science Inc; Domestic Animal Endocrinology; 61; 10-2017; 100-1070739-7240CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0739724017300127?via%3Dihubinfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.domaniend.2017.06.004info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:47:53Zoai:ri.conicet.gov.ar:11336/51198instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:47:53.672CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
title Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
spellingShingle Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
Recabarren, S. E.
Amh
Developmental Programming
Germ Cells
Pcos
Sertoli Cells
Testicle
title_short Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
title_full Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
title_fullStr Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
title_full_unstemmed Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
title_sort Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone
dc.creator.none.fl_str_mv Recabarren, S. E.
Recabarren, Mónica
Sandoval, D.
Carrasco, A.
Padmanabhan, Vasantha
Rey, Rodolfo Alberto
Richter, Hans
Perez Marin, C. C.
Sir Petermann, Teresa
Rojas Garcia, P.P.
author Recabarren, S. E.
author_facet Recabarren, S. E.
Recabarren, Mónica
Sandoval, D.
Carrasco, A.
Padmanabhan, Vasantha
Rey, Rodolfo Alberto
Richter, Hans
Perez Marin, C. C.
Sir Petermann, Teresa
Rojas Garcia, P.P.
author_role author
author2 Recabarren, Mónica
Sandoval, D.
Carrasco, A.
Padmanabhan, Vasantha
Rey, Rodolfo Alberto
Richter, Hans
Perez Marin, C. C.
Sir Petermann, Teresa
Rojas Garcia, P.P.
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Amh
Developmental Programming
Germ Cells
Pcos
Sertoli Cells
Testicle
topic Amh
Developmental Programming
Germ Cells
Pcos
Sertoli Cells
Testicle
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The male gonadal tissue can be a sensitive target to the reprogramming effects of testosterone (T) during prenatal development. We have demonstrated that male lambs born to dams receiving T during pregnancyda model system to the polycystic ovary syndrome (PCOS)d show a decreased number of germ cells early in life, and when adult, a reduced amount of sperm and ejaculate volume. These findings are a key to put attention to the male offspring of women bearing PCOS, as they are exposed to increased levels of androgen during pregnancy which can reprogram their reproductive outcome. A possible origin of these defects can be a disruption in the expression of the anti-Müllerian hormone (AMH), due to its critical role in gonadal function at many postnatal stages. Therefore, we addressed the impact of prenatal T excess on the expression of AMH and factors related to its expression like AP2, SOX9, FSHR, and AR in the testicular tissue through real-time PCR during the peripubertal age. We also analyzed the testicular morphology and quantified the number of Sertoli cells and germ cells to evaluate any further defect in the testicle. Experiments were performed in rams at 24 wk of age, hence, prior puberty. The experimental animals (T-males) consisted of rams born to mothers receiving 30 mg testosterone twice a wk from Day 30 to 90 of pregnancy and then increased to 40 mg until Day 120 of pregnancy. The control males (C-males) were born to mothers receiving the vehicle of the hormone. We found a significant increase in the expression of the mRNA of AMH and SOX9, but not of the AP2, FHSR nor AR, in the T-males. Moreover, T-males showed a dramatic decrease in the number of germ cells, together with a decrease in the weight of their testicles. The findings of the present study show that before puberty, T-males are manifesting clear signs of disruption in the gonadal functions probably due to an alteration in the expression pattern of the AMH gene. The precise way by which T reprograms the expression of AMH gene remains to be established.
Fil: Recabarren, S. E.. Universidad de Concepción; Chile
Fil: Recabarren, Mónica. Universidad de Concepción; Chile
Fil: Sandoval, D.. Universidad de Concepción; Chile
Fil: Carrasco, A.. Universidad de Concepción; Chile
Fil: Padmanabhan, Vasantha. University of Michigan; Estados Unidos
Fil: Rey, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas ; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Richter, Hans. Universidad Austral de Chile; Chile
Fil: Perez Marin, C. C.. Universidad de Córdoba; España
Fil: Sir Petermann, Teresa. Universidad de Chile; Chile
Fil: Rojas Garcia, P.P.. Universidad de Concepción; Chile
description The male gonadal tissue can be a sensitive target to the reprogramming effects of testosterone (T) during prenatal development. We have demonstrated that male lambs born to dams receiving T during pregnancyda model system to the polycystic ovary syndrome (PCOS)d show a decreased number of germ cells early in life, and when adult, a reduced amount of sperm and ejaculate volume. These findings are a key to put attention to the male offspring of women bearing PCOS, as they are exposed to increased levels of androgen during pregnancy which can reprogram their reproductive outcome. A possible origin of these defects can be a disruption in the expression of the anti-Müllerian hormone (AMH), due to its critical role in gonadal function at many postnatal stages. Therefore, we addressed the impact of prenatal T excess on the expression of AMH and factors related to its expression like AP2, SOX9, FSHR, and AR in the testicular tissue through real-time PCR during the peripubertal age. We also analyzed the testicular morphology and quantified the number of Sertoli cells and germ cells to evaluate any further defect in the testicle. Experiments were performed in rams at 24 wk of age, hence, prior puberty. The experimental animals (T-males) consisted of rams born to mothers receiving 30 mg testosterone twice a wk from Day 30 to 90 of pregnancy and then increased to 40 mg until Day 120 of pregnancy. The control males (C-males) were born to mothers receiving the vehicle of the hormone. We found a significant increase in the expression of the mRNA of AMH and SOX9, but not of the AP2, FHSR nor AR, in the T-males. Moreover, T-males showed a dramatic decrease in the number of germ cells, together with a decrease in the weight of their testicles. The findings of the present study show that before puberty, T-males are manifesting clear signs of disruption in the gonadal functions probably due to an alteration in the expression pattern of the AMH gene. The precise way by which T reprograms the expression of AMH gene remains to be established.
publishDate 2017
dc.date.none.fl_str_mv 2017-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/51198
Recabarren, S. E.; Recabarren, Mónica; Sandoval, D.; Carrasco, A.; Padmanabhan, Vasantha; et al.; Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone; Elsevier Science Inc; Domestic Animal Endocrinology; 61; 10-2017; 100-107
0739-7240
CONICET Digital
CONICET
url http://hdl.handle.net/11336/51198
identifier_str_mv Recabarren, S. E.; Recabarren, Mónica; Sandoval, D.; Carrasco, A.; Padmanabhan, Vasantha; et al.; Puberty arises with testicular alterations and defective AMH expression in rams prenatally exposed to testosterone; Elsevier Science Inc; Domestic Animal Endocrinology; 61; 10-2017; 100-107
0739-7240
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0739724017300127?via%3Dihub
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.domaniend.2017.06.004
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science Inc
publisher.none.fl_str_mv Elsevier Science Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842268888563187712
score 13.13397

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