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Maternal malnutrition associated with postnatal sugar consumption increases inflammatory response and prostate disorders in rat offspring

dc.contributor.authorNaia Fioretto, Matheus [UNESP]
dc.contributor.authorColombelli, Ketlin Thassiani [UNESP]
dc.contributor.authorda Silva, Cecilia Luvizutti Ferreira [UNESP]
dc.contributor.authordos Santos, Sérgio Alexandre Alcantara [UNESP]
dc.contributor.authorCamargo, Ana Carolina Lima [UNESP]
dc.contributor.authorConstantino, Flávia Bessi [UNESP]
dc.contributor.authorPortela, Luiz Marcos Frediani [UNESP]
dc.contributor.authorAquino, Ariana Musa de [UNESP]
dc.contributor.authorBarata, Luisa Annibal [UNESP]
dc.contributor.authorMattos, Renato [UNESP]
dc.contributor.authorScarano, Wellerson Rodrigo [UNESP]
dc.contributor.authorZambrano, Elena
dc.contributor.authorJustulin, Luis Antonio [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionFox Chase Cancer Center
dc.contributor.institutionInstituto Nacional de Ciencias Médicas y Nutrición
dc.contributor.institutionUniversidad Nacional Autónoma de México
dc.date.accessioned2025-04-29T20:10:33Z
dc.date.issued2024-07-01
dc.description.abstractMaternal malnutrition can alter developmental biology, programming health and disease in offspring. The increase in sugar consumption during the peripubertal period, a worldwide concern, also affects health through adulthood. Studies have shown that maternal exposure to a low protein diet (LPD) is associated with an increase in prostate disease with aging. However, the combined effects of maternal LPD and early postnatal sugar consumption on offspring prostate disorders were not investigated. The effects on aging were evaluated using a maternal gestational model with lactational LPD (6% protein) and sugar consumption (10%) from postnatal day (PND) 21–90, associating the consequences on ventral prostate (VP) rats morphophysiology on PND540. An increase was shown in mast cells and in the VP of the CTR + SUG and Gestational and Lactational Low Protein (GLLP) groups. In GLLP + SUG, a significant increase was shown in TGF-β1 expression in both the systemic and intra-prostatic forms, and SMAD2/3p had increased. The study identified maternal LPD and sugar consumption as risk factors for prostatic homeostasis in senility, activating the TGFβ1-SMAD2/3 pathway, a signaling pathway with potential markers for prostatic disorders.en
dc.description.affiliationDepartment of Structural and Functional Biology Institute of Biosciences Sao Paulo State University, SP
dc.description.affiliationCancer Signaling and Epigenetics Program Fox Chase Cancer Center
dc.description.affiliationDepartamento de Biología de la Reproducción Instituto Nacional de Ciencias Médicas y Nutrición
dc.description.affiliationFacultad de Química Universidad Nacional Autónoma de México
dc.description.affiliationUnespDepartment of Structural and Functional Biology Institute of Biosciences Sao Paulo State University, SP
dc.identifierhttp://dx.doi.org/10.1016/j.mce.2024.112223
dc.identifier.citationMolecular and Cellular Endocrinology, v. 588.
dc.identifier.doi10.1016/j.mce.2024.112223
dc.identifier.issn1872-8057
dc.identifier.issn0303-7207
dc.identifier.scopus2-s2.0-85189544386
dc.identifier.urihttps://hdl.handle.net/11449/307887
dc.language.isoeng
dc.relation.ispartofMolecular and Cellular Endocrinology
dc.sourceScopus
dc.subjectInflammation
dc.subjectMaternal malnutrition
dc.subjectProstate disorders
dc.subjectSugar
dc.subjectTGFβ1-SMAD2/3
dc.titleMaternal malnutrition associated with postnatal sugar consumption increases inflammatory response and prostate disorders in rat offspringen
dc.typeArtigopt
dspace.entity.typePublication
unesp.author.orcid0000-0002-2711-6359[2]
unesp.author.orcid0000-0002-1375-1634 0000-0002-1375-1634[4]
unesp.author.orcid0000-0002-5898-3615[7]
unesp.author.orcid0000-0002-2491-4443[10]
unesp.author.orcid0000-0002-6682-2934[11]

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