Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects

Autores
Perez Perez, Antonio; Guadix, P.; Maymo, Julieta Lorena; Dueñas, Jose Luis; Varone, Cecilia Laura; Sanchez Margalet, M; Sanchez Margalet, V.
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation.
Fil: Perez Perez, Antonio. Hospital Virgen Macarena; España
Fil: Guadix, P.. Hospital Virgen Macarena; España. Hospital Virgen Macarena; España
Fil: Maymo, Julieta Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Dueñas, Jose Luis. Departamento de Bioquímica Médica y Biología Molecular; España
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Sanchez Margalet, M. IVI Sevilla; España
Fil: Sanchez Margalet, V.. Hospital Virgen Macarena; España
Materia
Gestational Diabetes
Insulin
Leptin
Placenta
Signal Transduction
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:11336/49150
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/49150
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Insulin and Leptin Signaling in Placenta from Gestational Diabetic SubjectsPerez Perez, AntonioGuadix, P.Maymo, Julieta LorenaDueñas, Jose LuisVarone, Cecilia LauraSanchez Margalet, MSanchez Margalet, V.Gestational DiabetesInsulinLeptinPlacentaSignal Transductionhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation.Fil: Perez Perez, Antonio. Hospital Virgen Macarena; EspañaFil: Guadix, P.. Hospital Virgen Macarena; España. Hospital Virgen Macarena; EspañaFil: Maymo, Julieta Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Dueñas, Jose Luis. Departamento de Bioquímica Médica y Biología Molecular; EspañaFil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Sanchez Margalet, M. IVI Sevilla; EspañaFil: Sanchez Margalet, V.. Hospital Virgen Macarena; EspañaGeorg Thieme Verlag Kg2015-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/49150Perez Perez, Antonio; Guadix, P.; Maymo, Julieta Lorena; Dueñas, Jose Luis; Varone, Cecilia Laura; et al.; Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects; Georg Thieme Verlag Kg; Hormone and Metabolic Research; 48; 1; 11-2015; 62-690018-5043CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1055/s-0035-1559722info:eu-repo/semantics/altIdentifier/url/https://www.thieme-connect.de/DOI/DOI?10.1055/s-0035-1559722info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:05:26Zoai:ri.conicet.gov.ar:11336/49150instacron: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 10:05:26.838CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
title Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
spellingShingle Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
Perez Perez, Antonio
Gestational Diabetes
Insulin
Leptin
Placenta
Signal Transduction
title_short Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
title_full Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
title_fullStr Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
title_full_unstemmed Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
title_sort Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
dc.creator.none.fl_str_mv Perez Perez, Antonio
Guadix, P.
Maymo, Julieta Lorena
Dueñas, Jose Luis
Varone, Cecilia Laura
Sanchez Margalet, M
Sanchez Margalet, V.
author Perez Perez, Antonio
author_facet Perez Perez, Antonio
Guadix, P.
Maymo, Julieta Lorena
Dueñas, Jose Luis
Varone, Cecilia Laura
Sanchez Margalet, M
Sanchez Margalet, V.
author_role author
author2 Guadix, P.
Maymo, Julieta Lorena
Dueñas, Jose Luis
Varone, Cecilia Laura
Sanchez Margalet, M
Sanchez Margalet, V.
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Gestational Diabetes
Insulin
Leptin
Placenta
Signal Transduction
topic Gestational Diabetes
Insulin
Leptin
Placenta
Signal Transduction
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation.
Fil: Perez Perez, Antonio. Hospital Virgen Macarena; España
Fil: Guadix, P.. Hospital Virgen Macarena; España. Hospital Virgen Macarena; España
Fil: Maymo, Julieta Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Dueñas, Jose Luis. Departamento de Bioquímica Médica y Biología Molecular; España
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Sanchez Margalet, M. IVI Sevilla; España
Fil: Sanchez Margalet, V.. Hospital Virgen Macarena; España
description Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation.
publishDate 2015
dc.date.none.fl_str_mv 2015-11
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/11336/49150
Perez Perez, Antonio; Guadix, P.; Maymo, Julieta Lorena; Dueñas, Jose Luis; Varone, Cecilia Laura; et al.; Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects; Georg Thieme Verlag Kg; Hormone and Metabolic Research; 48; 1; 11-2015; 62-69
0018-5043
CONICET Digital
CONICET
url http://hdl.handle.net/11336/49150
identifier_str_mv Perez Perez, Antonio; Guadix, P.; Maymo, Julieta Lorena; Dueñas, Jose Luis; Varone, Cecilia Laura; et al.; Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects; Georg Thieme Verlag Kg; Hormone and Metabolic Research; 48; 1; 11-2015; 62-69
0018-5043
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1055/s-0035-1559722
info:eu-repo/semantics/altIdentifier/url/https://www.thieme-connect.de/DOI/DOI?10.1055/s-0035-1559722
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 Georg Thieme Verlag Kg
publisher.none.fl_str_mv Georg Thieme Verlag Kg
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
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score 13.13397

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