Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1007/s43032-023-01198-9 http://hdl.handle.net/11449/248430 |
Resumo: | We used uncontrolled maternal diabetes as a model to provoke fetal growth restriction in the female in the first generation (F1) and to evaluate reproductive outcomes and the possible changes in metabolic systems during pregnancy, as well as the repercussions at birth in the second generation (F2). For this, nondiabetic and streptozotocin-induced severely diabetic Sprague-Dawley rats were mated to obtain female pups (F1), which were classified as adequate (AGA) or small (SGA) for gestational weight. Afterward, we composed two groups: F1 AGA from nondiabetic dams (Control) and F1 SGA from severely diabetic dams (Restricted) (n minimum = 10 animals/groups). At adulthood, these rats were submitted to the oral glucose tolerance test, mated, and at day 17 of pregnancy, blood samples were collected to determine glucose and insulin levels for assessment of insulin resistance. At the end of the pregnancy, the blood and liver samples were collected to evaluate redox status markers, and reproductive, fetal, and placental outcomes were analyzed. Maternal diabetes was responsible for increased SGA rates and a lower percentage of AGA fetuses (F1 generation). The restricted female pups from severely diabetic dams presented rapid neonatal catch-up growth, glucose intolerance, and insulin resistance status before and during pregnancy. At term pregnancy of F1 generation, oxidative stress status was observed in the maternal liver and blood samples. In addition, their offspring (F2 generation) had lower fetal weight and placental efficiency, regardless of gender, which caused fetal growth restriction and confirmed the fetal programming influence. |
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Severe Diabetes Induction as a Generational Model for Growth Restriction of RatAnimal modelsFetal programmingHyperglycemiaLow birth weightMalondialdehydePregnancyWe used uncontrolled maternal diabetes as a model to provoke fetal growth restriction in the female in the first generation (F1) and to evaluate reproductive outcomes and the possible changes in metabolic systems during pregnancy, as well as the repercussions at birth in the second generation (F2). For this, nondiabetic and streptozotocin-induced severely diabetic Sprague-Dawley rats were mated to obtain female pups (F1), which were classified as adequate (AGA) or small (SGA) for gestational weight. Afterward, we composed two groups: F1 AGA from nondiabetic dams (Control) and F1 SGA from severely diabetic dams (Restricted) (n minimum = 10 animals/groups). At adulthood, these rats were submitted to the oral glucose tolerance test, mated, and at day 17 of pregnancy, blood samples were collected to determine glucose and insulin levels for assessment of insulin resistance. At the end of the pregnancy, the blood and liver samples were collected to evaluate redox status markers, and reproductive, fetal, and placental outcomes were analyzed. Maternal diabetes was responsible for increased SGA rates and a lower percentage of AGA fetuses (F1 generation). The restricted female pups from severely diabetic dams presented rapid neonatal catch-up growth, glucose intolerance, and insulin resistance status before and during pregnancy. At term pregnancy of F1 generation, oxidative stress status was observed in the maternal liver and blood samples. In addition, their offspring (F2 generation) had lower fetal weight and placental efficiency, regardless of gender, which caused fetal growth restriction and confirmed the fetal programming influence.Postgraduate Course on Tocogynecology Laboratory of Experimental Research on Gynecology and Obstetrics Botucatu Medical School São Paulo State University (UNESP), São Paulo StateInstitute of Biological and Health Sciences Laboratory of System Physiology and Reproductive Toxicology Federal University of Mato Grosso (UFMT), Mato Grosso StateResearch Support Office Botucatu Medical School Sao Paulo State University (UNESP), São Paulo StateInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán Department of Reproductive BiologyPostgraduate Course on Tocogynecology Laboratory of Experimental Research on Gynecology and Obstetrics Botucatu Medical School São Paulo State University (UNESP), São Paulo StateResearch Support Office Botucatu Medical School Sao Paulo State University (UNESP), São Paulo StateUniversidade Estadual Paulista (UNESP)Federal University of Mato Grosso (UFMT)Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubiránda Cruz, Larissa Lopes [UNESP]Barco, Vinícius Soares [UNESP]Paula, Verônyca Gonçalves [UNESP]Gallego, Franciane Quintanilha [UNESP]Souza, Maysa Rocha [UNESP]Corrente, José Eduardo [UNESP]Zambrano, ElenaVolpato, Gustavo TadeuDamasceno, Débora Cristina [UNESP]2023-07-29T13:43:52Z2023-07-29T13:43:52Z2023-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1007/s43032-023-01198-9Reproductive Sciences.1933-72051933-7191http://hdl.handle.net/11449/24843010.1007/s43032-023-01198-92-s2.0-85149030944Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengReproductive Sciencesinfo:eu-repo/semantics/openAccess2023-07-29T13:43:52Zoai:repositorio.unesp.br:11449/248430Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462023-07-29T13:43:52Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
title |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
spellingShingle |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat da Cruz, Larissa Lopes [UNESP] Animal models Fetal programming Hyperglycemia Low birth weight Malondialdehyde Pregnancy |
title_short |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
title_full |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
title_fullStr |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
title_full_unstemmed |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
title_sort |
Severe Diabetes Induction as a Generational Model for Growth Restriction of Rat |
author |
da Cruz, Larissa Lopes [UNESP] |
author_facet |
da Cruz, Larissa Lopes [UNESP] Barco, Vinícius Soares [UNESP] Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Souza, Maysa Rocha [UNESP] Corrente, José Eduardo [UNESP] Zambrano, Elena Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
author_role |
author |
author2 |
Barco, Vinícius Soares [UNESP] Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Souza, Maysa Rocha [UNESP] Corrente, José Eduardo [UNESP] Zambrano, Elena Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
author2_role |
author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (UNESP) Federal University of Mato Grosso (UFMT) Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán |
dc.contributor.author.fl_str_mv |
da Cruz, Larissa Lopes [UNESP] Barco, Vinícius Soares [UNESP] Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Souza, Maysa Rocha [UNESP] Corrente, José Eduardo [UNESP] Zambrano, Elena Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
dc.subject.por.fl_str_mv |
Animal models Fetal programming Hyperglycemia Low birth weight Malondialdehyde Pregnancy |
topic |
Animal models Fetal programming Hyperglycemia Low birth weight Malondialdehyde Pregnancy |
description |
We used uncontrolled maternal diabetes as a model to provoke fetal growth restriction in the female in the first generation (F1) and to evaluate reproductive outcomes and the possible changes in metabolic systems during pregnancy, as well as the repercussions at birth in the second generation (F2). For this, nondiabetic and streptozotocin-induced severely diabetic Sprague-Dawley rats were mated to obtain female pups (F1), which were classified as adequate (AGA) or small (SGA) for gestational weight. Afterward, we composed two groups: F1 AGA from nondiabetic dams (Control) and F1 SGA from severely diabetic dams (Restricted) (n minimum = 10 animals/groups). At adulthood, these rats were submitted to the oral glucose tolerance test, mated, and at day 17 of pregnancy, blood samples were collected to determine glucose and insulin levels for assessment of insulin resistance. At the end of the pregnancy, the blood and liver samples were collected to evaluate redox status markers, and reproductive, fetal, and placental outcomes were analyzed. Maternal diabetes was responsible for increased SGA rates and a lower percentage of AGA fetuses (F1 generation). The restricted female pups from severely diabetic dams presented rapid neonatal catch-up growth, glucose intolerance, and insulin resistance status before and during pregnancy. At term pregnancy of F1 generation, oxidative stress status was observed in the maternal liver and blood samples. In addition, their offspring (F2 generation) had lower fetal weight and placental efficiency, regardless of gender, which caused fetal growth restriction and confirmed the fetal programming influence. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023-07-29T13:43:52Z 2023-07-29T13:43:52Z 2023-01-01 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1007/s43032-023-01198-9 Reproductive Sciences. 1933-7205 1933-7191 http://hdl.handle.net/11449/248430 10.1007/s43032-023-01198-9 2-s2.0-85149030944 |
url |
http://dx.doi.org/10.1007/s43032-023-01198-9 http://hdl.handle.net/11449/248430 |
identifier_str_mv |
Reproductive Sciences. 1933-7205 1933-7191 10.1007/s43032-023-01198-9 2-s2.0-85149030944 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Reproductive Sciences |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1799965092535599104 |