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Effect of maternal obesity on diabetes development in adult rat offspring

dc.contributor.authorCampos, Kleber Eduardo de [UNESP]
dc.contributor.authorSinzato, Yuri Karen
dc.contributor.authorPimenta, Walkyria de Paula
dc.contributor.authorRudge, Marilza Vieira Cunha [UNESP]
dc.contributor.authorDamasceno, Debora Cristina
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:28:53Z
dc.date.available2014-05-20T15:28:53Z
dc.date.issued2007-10-27
dc.description.abstractThis study aimed to evaluate whether maternal obesity leads to the onset of diabetes in adult Wistar rats offspring. MSG solution neonatally administration induced obesity in rats (F(1)MSG group, n = 30); and saline solution was also administrated to control rats (F1CON group, n = 13). In 3rd month of age, both control and MS G groups were mated for offspring (generation FA named as F2CON, n = 28 and F(2)MSG groups, n = 15; and so both generations were studied until 7th month of life. Lee Index was measured for experimental obesity validation from 5th to 7th month. Glycemia was weekly determined during pregnancy and monthly from 3rd to 7th month. In the end of experimental period all rats were submitted to oral glucose tolerance test (OGTT), with estimation of total area under the curve (AUC); and insulin tolerance test (ITT). Rats were then anesthetized and killed. Data were statistically analyzed with significance level of p < 0.05. Lee Index has confirmed obesity in all MSG rats. Glycemic levels comparisons between generations showed significant maternal interference in control and MSG groups. OGTT analysis showed higher glycemia in obese rats (F(1)MSG) and their offspring (F(2)MSG) as compared to their respective controls; and MSG groups increased AUC from OGTT. As regards ITT, F(2)MSG showed higher glycemia at 30 and 120 min, suggesting a delay of insulin action decreasing. Although glucose intolerance and insulin resistance clinical conditions represent as a factors for type 2 Diabetes mellitus development, this experimental model proposal was not efficient to induce type 2 Diabetes mellitus, but for obesity developing, glucose intolerance and insulin resistance in successive generations of rats. (c) 2007 Elsevier B.V. All rights reserved.en
dc.description.affiliationSão Paulo State Univ, Sch Med, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Sch Med, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, BR-18618000 Botucatu, SP, Brazil
dc.format.extent1473-1478
dc.identifierhttp://dx.doi.org/10.1016/j.lfs.2007.09.016
dc.identifier.citationLife Sciences. Oxford: Pergamon-Elsevier B.V., v. 81, n. 19-20, p. 1473-1478, 2007.
dc.identifier.doi10.1016/j.lfs.2007.09.016
dc.identifier.issn0024-3205
dc.identifier.lattes6758680388835078
dc.identifier.orcid0000-0002-9227-832X
dc.identifier.urihttp://hdl.handle.net/11449/38611
dc.identifier.wosWOS:000251362500010
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofLife Sciences
dc.relation.ispartofjcr3.234
dc.relation.ispartofsjr1,071
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectobesitypt
dc.subjectmonosodium glutamatept
dc.subjectoffspringpt
dc.subjectdiabetespt
dc.subjectpregnancypt
dc.titleEffect of maternal obesity on diabetes development in adult rat offspringen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
unesp.author.lattes6758680388835078
unesp.author.orcid0000-0002-7003-9643[5]
unesp.author.orcid0000-0002-9227-832X[4]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
unesp.departmentGinecologia e Obstetrícia - FMBpt

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