Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta

Autores
Jawerbaum, Alicia Sandra; Capobianco, Evangelina Lorena; Martinez, Nora Alicia; White, Verónica; Pustovrh, María Carolina; Higa, Romina Daniela; Gonzalez, Élida Teresa
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
OBJECTIVE: Peroxisome proliferator activated receptors (PPARs), known regulators of lipid homeostasis in different tissues, are crucial during placental development. In this work we aim to determine whether PPARs activation modulates lipid metabolism in the placenta from control and diabetic experimental models at midgestation. MATERIALS-METHODS: Placental explants obtained from control and neonatal-streptozotocin-induced- diabetic rats on day 13.5 of gestation were cultured in the presence or absence of ligands of the three PPARs isoforms (clofibrate, 15deoxydelta12,14prostaglandin J2 and carbaprostacyclin; which are PPARα, PPARγ and PPARδ agonists respectively) for further analysis of lipid metabolism. Lipid levels (triglycerides, cholesterol, cholesteryl esters and phospholipids) were analysed by thin layer chromatography, de novo lipid synthesis was assessed by incorporation of 14C-acetate as a tracer, and lipid catabolism was studied through the evaluation of glycerol release. RESULTS: Placental tissues from diabetic rats showed increased triglycerides and cholesteryl ester levels, decreased de novo lipid synthesis and enhanced lipid catabolism when compared to controls. PPARα activation reduced lipid levels and synthesis, and increased lipid catabolism in the placenta. PPARγ activation did not modify placental lipid mass and catabolism, but significantly reduced de novo lipid synthesis. PPARδ ligands reduced phospholipid levels and de novo lipid synthesis, and increased placental lipid catabolism. CONCLUSIONS: These results provide evidence of novel PPARs functions as regulators of placental lipid metabolism, a first step in the understanding of pathways that may allow the regulation of placental lipid metabolism and the prevention of the lipid overload transferred to the developing fetus in maternal diabetes.
Fil: Jawerbaum, Alicia Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Capobianco, Evangelina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Martinez, Nora Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: White, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Pustovrh, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Higa, Romina Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Gonzalez, Élida Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Materia
Diabetes
Placenta
Ppars
Lipids
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:11336/20735
Acceder
id CONICETDig_a9bdb3abb4582bd3aba00f76c9910762
oai_identifier_str oai:ri.conicet.gov.ar:11336/20735
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placentaJawerbaum, Alicia SandraCapobianco, Evangelina LorenaMartinez, Nora AliciaWhite, VerónicaPustovrh, María CarolinaHiga, Romina DanielaGonzalez, Élida TeresaDiabetesPlacentaPparsLipidshttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3OBJECTIVE: Peroxisome proliferator activated receptors (PPARs), known regulators of lipid homeostasis in different tissues, are crucial during placental development. In this work we aim to determine whether PPARs activation modulates lipid metabolism in the placenta from control and diabetic experimental models at midgestation. MATERIALS-METHODS: Placental explants obtained from control and neonatal-streptozotocin-induced- diabetic rats on day 13.5 of gestation were cultured in the presence or absence of ligands of the three PPARs isoforms (clofibrate, 15deoxydelta12,14prostaglandin J2 and carbaprostacyclin; which are PPARα, PPARγ and PPARδ agonists respectively) for further analysis of lipid metabolism. Lipid levels (triglycerides, cholesterol, cholesteryl esters and phospholipids) were analysed by thin layer chromatography, de novo lipid synthesis was assessed by incorporation of 14C-acetate as a tracer, and lipid catabolism was studied through the evaluation of glycerol release. RESULTS: Placental tissues from diabetic rats showed increased triglycerides and cholesteryl ester levels, decreased de novo lipid synthesis and enhanced lipid catabolism when compared to controls. PPARα activation reduced lipid levels and synthesis, and increased lipid catabolism in the placenta. PPARγ activation did not modify placental lipid mass and catabolism, but significantly reduced de novo lipid synthesis. PPARδ ligands reduced phospholipid levels and de novo lipid synthesis, and increased placental lipid catabolism. CONCLUSIONS: These results provide evidence of novel PPARs functions as regulators of placental lipid metabolism, a first step in the understanding of pathways that may allow the regulation of placental lipid metabolism and the prevention of the lipid overload transferred to the developing fetus in maternal diabetes.Fil: Jawerbaum, Alicia Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Capobianco, Evangelina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Martinez, Nora Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: White, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Pustovrh, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Higa, Romina Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Gonzalez, Élida Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaGalenos Yayincilik2007-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/20735Jawerbaum, Alicia Sandra; Capobianco, Evangelina Lorena; Martinez, Nora Alicia; White, Verónica; Pustovrh, María Carolina; et al.; Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta; Galenos Yayincilik; Journal of the Turkish-German Gynecological Association; 8; 3; 9-2007; 249-2531309-03991309-0380CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.jtgga.org/search-result?search=Activation%20of%20Peroxisome%20Proliferator%20Nuclear%20Receptors%20Regulates%20Lipid%20Metabolism%20in%20the%20Placentainfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:32:43Zoai:ri.conicet.gov.ar:11336/20735instacron: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:34982025-10-15 15:32:43.305CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
title Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
spellingShingle Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
Jawerbaum, Alicia Sandra
Diabetes
Placenta
Ppars
Lipids
title_short Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
title_full Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
title_fullStr Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
title_full_unstemmed Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
title_sort Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta
dc.creator.none.fl_str_mv Jawerbaum, Alicia Sandra
Capobianco, Evangelina Lorena
Martinez, Nora Alicia
White, Verónica
Pustovrh, María Carolina
Higa, Romina Daniela
Gonzalez, Élida Teresa
author Jawerbaum, Alicia Sandra
author_facet Jawerbaum, Alicia Sandra
Capobianco, Evangelina Lorena
Martinez, Nora Alicia
White, Verónica
Pustovrh, María Carolina
Higa, Romina Daniela
Gonzalez, Élida Teresa
author_role author
author2 Capobianco, Evangelina Lorena
Martinez, Nora Alicia
White, Verónica
Pustovrh, María Carolina
Higa, Romina Daniela
Gonzalez, Élida Teresa
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Diabetes
Placenta
Ppars
Lipids
topic Diabetes
Placenta
Ppars
Lipids
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv OBJECTIVE: Peroxisome proliferator activated receptors (PPARs), known regulators of lipid homeostasis in different tissues, are crucial during placental development. In this work we aim to determine whether PPARs activation modulates lipid metabolism in the placenta from control and diabetic experimental models at midgestation. MATERIALS-METHODS: Placental explants obtained from control and neonatal-streptozotocin-induced- diabetic rats on day 13.5 of gestation were cultured in the presence or absence of ligands of the three PPARs isoforms (clofibrate, 15deoxydelta12,14prostaglandin J2 and carbaprostacyclin; which are PPARα, PPARγ and PPARδ agonists respectively) for further analysis of lipid metabolism. Lipid levels (triglycerides, cholesterol, cholesteryl esters and phospholipids) were analysed by thin layer chromatography, de novo lipid synthesis was assessed by incorporation of 14C-acetate as a tracer, and lipid catabolism was studied through the evaluation of glycerol release. RESULTS: Placental tissues from diabetic rats showed increased triglycerides and cholesteryl ester levels, decreased de novo lipid synthesis and enhanced lipid catabolism when compared to controls. PPARα activation reduced lipid levels and synthesis, and increased lipid catabolism in the placenta. PPARγ activation did not modify placental lipid mass and catabolism, but significantly reduced de novo lipid synthesis. PPARδ ligands reduced phospholipid levels and de novo lipid synthesis, and increased placental lipid catabolism. CONCLUSIONS: These results provide evidence of novel PPARs functions as regulators of placental lipid metabolism, a first step in the understanding of pathways that may allow the regulation of placental lipid metabolism and the prevention of the lipid overload transferred to the developing fetus in maternal diabetes.
Fil: Jawerbaum, Alicia Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Capobianco, Evangelina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Martinez, Nora Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: White, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Pustovrh, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Higa, Romina Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Gonzalez, Élida Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
description OBJECTIVE: Peroxisome proliferator activated receptors (PPARs), known regulators of lipid homeostasis in different tissues, are crucial during placental development. In this work we aim to determine whether PPARs activation modulates lipid metabolism in the placenta from control and diabetic experimental models at midgestation. MATERIALS-METHODS: Placental explants obtained from control and neonatal-streptozotocin-induced- diabetic rats on day 13.5 of gestation were cultured in the presence or absence of ligands of the three PPARs isoforms (clofibrate, 15deoxydelta12,14prostaglandin J2 and carbaprostacyclin; which are PPARα, PPARγ and PPARδ agonists respectively) for further analysis of lipid metabolism. Lipid levels (triglycerides, cholesterol, cholesteryl esters and phospholipids) were analysed by thin layer chromatography, de novo lipid synthesis was assessed by incorporation of 14C-acetate as a tracer, and lipid catabolism was studied through the evaluation of glycerol release. RESULTS: Placental tissues from diabetic rats showed increased triglycerides and cholesteryl ester levels, decreased de novo lipid synthesis and enhanced lipid catabolism when compared to controls. PPARα activation reduced lipid levels and synthesis, and increased lipid catabolism in the placenta. PPARγ activation did not modify placental lipid mass and catabolism, but significantly reduced de novo lipid synthesis. PPARδ ligands reduced phospholipid levels and de novo lipid synthesis, and increased placental lipid catabolism. CONCLUSIONS: These results provide evidence of novel PPARs functions as regulators of placental lipid metabolism, a first step in the understanding of pathways that may allow the regulation of placental lipid metabolism and the prevention of the lipid overload transferred to the developing fetus in maternal diabetes.
publishDate 2007
dc.date.none.fl_str_mv 2007-09
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/11336/20735
Jawerbaum, Alicia Sandra; Capobianco, Evangelina Lorena; Martinez, Nora Alicia; White, Verónica; Pustovrh, María Carolina; et al.; Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta; Galenos Yayincilik; Journal of the Turkish-German Gynecological Association; 8; 3; 9-2007; 249-253
1309-0399
1309-0380
CONICET Digital
CONICET
url http://hdl.handle.net/11336/20735
identifier_str_mv Jawerbaum, Alicia Sandra; Capobianco, Evangelina Lorena; Martinez, Nora Alicia; White, Verónica; Pustovrh, María Carolina; et al.; Activation of peroxisome proliferator nuclear receptors regulates lipid metabolism in the placenta; Galenos Yayincilik; Journal of the Turkish-German Gynecological Association; 8; 3; 9-2007; 249-253
1309-0399
1309-0380
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.jtgga.org/search-result?search=Activation%20of%20Peroxisome%20Proliferator%20Nuclear%20Receptors%20Regulates%20Lipid%20Metabolism%20in%20the%20Placenta
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 Galenos Yayincilik
publisher.none.fl_str_mv Galenos Yayincilik
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 13.22299

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