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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampLubaczeuski, Camila-
dc.contributor.authorunicampBoschiero, Antonio Carlos-
dc.typeArtigopt_BR
dc.titleMaternal Roux-en-Y gastric bypass impairs insulin action and endocrine pancreatic function in male F1 offspringpt_BR
dc.contributor.authorPietrobon, C.B.-
dc.contributor.authorBertasso, I.M.-
dc.contributor.authorRibeiro, R.A.-
dc.contributor.authorAlegre-Maller, A.C.P.-
dc.contributor.authorLubaczeuski, C.-
dc.contributor.authorBoschero, A.C.-
dc.contributor.authorAraújo, A.C.F.-
dc.contributor.authorBalbo, S.L.-
dc.contributor.authorBonfleur, M.L.-
dc.subjectDerivação gástricapt_BR
dc.subjectInsulinapt_BR
dc.subject.otherlanguageGastric bypasspt_BR
dc.subject.otherlanguageInsulinpt_BR
dc.description.abstractPurpose: Obesity is predominant in women of reproductive age. Roux-en-Y gastric bypass (RYGB) is the most common bariatric procedure that is performed in obese women for weight loss and metabolic improvement. However, some studies suggest that this procedure negatively affects offspring. Herein, using Western diet (WD)-obese female rats, we investigated the effects of maternal RYGB on postnatal body development, glucose tolerance, insulin secretion and action in their adult male F1 offspring. Methods: Female Wistar rats consumed a Western diet (WD) for 18 weeks, before being submitted to RYGB (WD-RYGB) or SHAM (WD-SHAM) operations. After 5 weeks, WD-RYGB and WD-SHAM females were mated with control male breeders, and the F1 offspring were identified as: WD-RYGB-F1 and WD-SHAM-F1. Results: The male F1 offspring of WD-RYGB dams exhibited decreased BW, but enhanced total nasoanal length gain. At 120 days of age, WD-RYGB-F1 rats displayed normal fasting glycemia and glucose tolerance but demonstrated reduced insulinemia and higher glucose disappearance after insulin stimulus. In addition, these rodents presented insulin resistance in the gastrocnemius muscle and retroperitoneal fat, as judged by lower Akt phosphorylation after insulin administration, but an increase in this protein in the liver. Finally, the islets from WD-RYGB-F1 rats secreted less insulin in response to glucose and displayed increased β-cell area and mass. Conclusions: RYGB in WD dams negatively affected their F1 offspring, leading to catch-up growth, insulin resistance in skeletal muscle and white fat, and β-cell dysfunction. Therefore, our data are the first to demonstrate that the RYGB in female rats may aggravate the metabolic imprinting induced by maternal WD consumption, in their male F1 descendants. However, since we only used male F1 rats, further studies are necessary to demonstrate if such effect may also occur in female F1 offspring from dams that underwent RYGB operation.pt_BR
dc.relation.ispartofEuropean journal of nutritionpt_BR
dc.relation.ispartofabbreviationEur. j. nutr.pt_BR
dc.publisher.cityBerlinpt_BR
dc.publisher.countryAlemanhapt_BR
dc.publisherSpringerpt_BR
dc.date.issued2019-
dc.date.monthofcirculationApr.pt_BR
dc.language.isoengpt_BR
dc.description.volume59pt_BR
dc.description.issuenumber3pt_BR
dc.description.firstpage1067pt_BR
dc.description.lastpage1079pt_BR
dc.rightsFechadopt_BR
dc.sourceScopuspt_BR
dc.identifier.issn1436-6207pt_BR
dc.identifier.eissn1436-6215pt_BR
dc.identifier.doi10.1007/s00394-019-01968-9pt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007/s00394-019-01968-9pt_BR
dc.date.available2020-05-14T18:10:41Z-
dc.date.accessioned2020-05-14T18:10:41Z-
dc.description.provenanceSubmitted by Bruna Maria Campos da Cunha (bcampos@unicamp.br) on 2020-05-14T18:10:41Z No. of bitstreams: 0. Added 1 bitstream(s) on 2020-08-27T19:17:55Z : No. of bitstreams: 1 2-s2.0-85064490220.pdf: 3550493 bytes, checksum: 00aedff3b13da628644b6c19f48cbb89 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-05-14T18:10:41Z (GMT). No. of bitstreams: 0 Previous issue date: 2019en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/341442-
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source2-s2.0-85064490220pt_BR
dc.creator.orcidorcid.org/0000-0001-6882-7686pt_BR
dc.creator.orcidorcid.org/0000-0003-3829-8570pt_BR
dc.type.formArtigo originalpt_BR
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