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dc.contributor.authorRinaldi, Jaqueline C.-
dc.contributor.authorJustulin Jr., Luis A.-
dc.contributor.authorLacorte, Livia M.-
dc.contributor.authorSarobo, Carolina-
dc.contributor.authorBoer, Patricia A.-
dc.contributor.authorScarano, Wellerson R.-
dc.contributor.authorFelisbino, Sergio L.-
dc.date.accessioned2014-05-27T11:28:56Z-
dc.date.accessioned2016-10-25T18:47:28Z-
dc.date.available2014-05-27T11:28:56Z-
dc.date.available2016-10-25T18:47:28Z-
dc.date.issued2013-04-19-
dc.identifierhttp://dx.doi.org/10.1016/j.lfs.2013.02.007-
dc.identifier.citationLife Sciences, v. 92, n. 13, p. 763-774, 2013.-
dc.identifier.issn0024-3205-
dc.identifier.issn1879-0631-
dc.identifier.urihttp://hdl.handle.net/11449/75136-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/75136-
dc.description.abstractAims Maternal malnutrition by low protein diet is associated with an increased incidence of metabolic disorders and decreased male fertility in adult life. This study aimed to assess the impact of maternal protein malnutrition (MPM) on prostate growth, tissue organization and lesion incidence with aging. Main methods Wistar rat dams were distributed into two groups, which were control (NP; fed a normal diet containing 17% protein) or a restricted protein diet (RP, fed a diet containing 6% protein) during gestation. After delivery all mothers and offspring received a normal diet. Biometrical parameters, hormonal levels and prostates were harvested at post-natal days (PND) 30, 120 and 360. Key findings MPM promoted low birth weight, decreased ano-genital distance (AGD) and reduced androgen plasma levels of male pups. Prostatic lobes from RP groups presented reduced glandular weight, epithelial cell height and alveolar diameter. The epithelial cell proliferation and collagen deposition were increased in RP group. Incidences of epithelial dysplasia and prostatitis were higher in the RP offspring than in the NP offspring at PND360. Significance Our findings show that MPM delays prostate development, growth and maturation until adulthood, probably as a result of low testosterone stimuli. The higher incidence of cellular dysplasia and prostatitis suggests that MPM increases prostate susceptibility to diseases with aging. © 2013 Elsevier Inc.en
dc.format.extent763-774-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectAndrogen receptor-
dc.subjectCollagen-
dc.subjectEpithelial dysplasia-
dc.subjectFetal programming-
dc.subjectProstatitis-
dc.subjectProtein malnutrition-
dc.subjectandrogen-
dc.subjectaging-
dc.subjectandrogen blood level-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectanimal tissue-
dc.subjectano genital distance-
dc.subjectcontrolled study-
dc.subjectdysplasia-
dc.subjectepithelial dysplasia-
dc.subjectfemale-
dc.subjectkwashiorkor-
dc.subjectlow birth weight-
dc.subjectmale-
dc.subjectmaternal disease-
dc.subjectmaternal protein malnutrition-
dc.subjectmaturation-
dc.subjectmeasurement-
dc.subjectnonhuman-
dc.subjectprogeny-
dc.subjectprostate-
dc.subjectprostatitis-
dc.subjectrat-
dc.subjectAging-
dc.subjectAnimals-
dc.subjectAnimals, Newborn-
dc.subjectApoptosis-
dc.subjectBody Weight-
dc.subjectDiet, Protein-Restricted-
dc.subjectEating-
dc.subjectFemale-
dc.subjectFetal Nutrition Disorders-
dc.subjectMale-
dc.subjectPregnancy-
dc.subjectProstate-
dc.subjectRats-
dc.subjectRats, Wistar-
dc.subjectReceptors, Androgen-
dc.subjectTestosterone-
dc.subjectRattus norvegicus-
dc.titleImplications of intrauterine protein malnutrition on prostate growth, maturation and agingen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Morphology Institute of Biosciences Univ Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Morphology School of Odontology Univ Estadual Paulista (UNESP)-
dc.description.affiliationUnespDepartment of Morphology Institute of Biosciences Univ Estadual Paulista (UNESP)-
dc.description.affiliationUnespDepartment of Morphology School of Odontology Univ Estadual Paulista (UNESP)-
dc.identifier.doi10.1016/j.lfs.2013.02.007-
dc.rights.accessRightsAcesso aberto-
dc.identifier.file2-s2.0-84875741455.pdf-
dc.relation.ispartofLife Sciences-
dc.identifier.scopus2-s2.0-84875741455-
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