Repercussions of mild diabetes on pregnancy in Wistar rats and on the fetal development

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dc.contributor.authorSaito, Felipe H. [UNESP]
dc.contributor.authorDamasceno, Débora Cristina [UNESP]
dc.contributor.authorKempinas, Wilma G. [UNESP]
dc.contributor.authorMorceli, Glilciane [UNESP]
dc.contributor.authorSinzato, Yuri K. [UNESP]
dc.contributor.authorTaylor, Kristin N. [UNESP]
dc.contributor.authorRudge, Marilza Vieira Cunha [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionWeill Cornell Med Coll
dc.date.accessioned2014-05-20T13:35:15Z
dc.date.available2014-05-20T13:35:15Z
dc.date.issued2010-04-23
dc.description.abstractBackground: Experimental models are necessary to elucidate diabetes pathophysiological mechanisms not yet understood in humans. Objective: To evaluate the repercussions of the mild diabetes, considering two methodologies, on the pregnancy of Wistar rats and on the development of their offspring.Methods: In the 1st induction, female offspring were distributed into two experimental groups: Group streptozotocin (STZ, n = 67): received the beta-cytotoxic agent (100 mg STZ/kg body weight - sc) on the 1st day of the life; and Nondiabetic Group (ND, n = 14): received the vehicle in a similar time period. In the adult life, the animals were mated. After a positive diagnosis of pregnancy (0), female rats from group STZ presenting with lower glycemia than 120 mg/dL received more 20 mg STZ/kg (ip) at day 7 of pregnancy (2nd induction). The female rats with glycemia higher than 120 mg/dL were discarded because they reproduced results already found in the literature. In the mornings of days 0, 7, 14 and 21 of the pregnancy glycemia was determined. At day 21 of pregnancy (at term), the female rats were anesthetized and killed for maternal reproductive performance and fetal development analysis. The data were analyzed using Student-Newman-Keuls, Chi-square and Zero-inflated Poisson (ZIP) Tests (p < 0.05).Results: STZ rats presented increased rates of pre (STZ = 22.0%; ND = 5.1%) and post-implantation losses (STZ = 26.1%; ND = 5.7%), reduced rates of fetuses with appropriate weight for gestational age (STZ = 66%; ND = 93%) and reduced degree of development (ossification sites).Conclusion: Mild diabetes led a negative impact on maternal reproductive performance and caused intrauterine growth restriction and impaired fetal development.en
dc.description.affiliationUniv Estadual Paulista, UNESP, Dept Gynecol & Obstet, Fac Med Botucatu,Lab Expt Res Gynecol & Obstet, São Paulo, SP, Brazil
dc.description.affiliationUniv Estadual Paulista, UNESP, Dept Morphol,Inst Biociencias Botucatu, Lab Biol & Toxicol Reprod Desenvolvimento ReproTo, São Paulo, SP, Brazil
dc.description.affiliationWeill Cornell Med Coll, New York, NY USA
dc.description.affiliationUnespUniv Estadual Paulista, UNESP, Dept Gynecol & Obstet, Fac Med Botucatu,Lab Expt Res Gynecol & Obstet, São Paulo, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, UNESP, Dept Morphol,Inst Biociencias Botucatu, Lab Biol & Toxicol Reprod Desenvolvimento ReproTo, São Paulo, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 08/00763-6
dc.format.extent8
dc.identifierhttp://dx.doi.org/10.1186/1758-5996-2-26
dc.identifier.citationDiabetology & Metabolic Syndrome. London: Biomed Central Ltd., v. 2, p. 8, 2010.
dc.identifier.doi10.1186/1758-5996-2-26
dc.identifier.fileWOS000290259400001.pdf
dc.identifier.issn1758-5996
dc.identifier.lattes6758680388835078
dc.identifier.orcid0000-0002-9227-832X
dc.identifier.urihttp://hdl.handle.net/11449/12114
dc.identifier.wosWOS:000290259400001
dc.language.isoeng
dc.publisherBiomed Central Ltd.
dc.relation.ispartofDiabetology & Metabolic Syndrome
dc.relation.ispartofjcr2.413
dc.relation.ispartofsjr0,943
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.titleRepercussions of mild diabetes on pregnancy in Wistar rats and on the fetal developmenten
dc.typeArtigo
dcterms.licensehttp://www.biomedcentral.com/about/license
dcterms.licensehttp://www.biomedcentral.com/about/license
dcterms.rightsHolderBiomed Central Ltd.
unesp.author.lattes6758680388835078
unesp.author.orcid0000-0002-7003-9643[2]
unesp.author.orcid0000-0002-2112-5123[3]
unesp.author.orcid0000-0002-9227-832X[7]
unesp.author.orcid0000-0001-8216-9931[4]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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Artigos - Ginecologia e Obstetrícia - FMB
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