Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.3389/fphys.2021.701767 http://hdl.handle.net/11449/229394 |
Resumo: | Embryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth. |
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Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of RatsbiochemicalhyperglycemiamalformationobesitypregnancyratEmbryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth.Laboratory of System Physiology and Reproductive Toxicology Institute of Biological and Health Sciences Federal University of Mato GrossoLaboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Program on Tocogynecology São Paulo State UniversityLaboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Program on Tocogynecology São Paulo State UniversityFederal University of Mato GrossoUniversidade Estadual Paulista (UNESP)Araujo-Silva, Vanessa CarulineSantos-Silva, AliceLourenço, Andressa SilvaBarros-Barbosa, Cristielly MariaMoraes-Souza, Rafaianne Queiroz [UNESP]Soares, Thaigra Sousa [UNESP]Karki, Barshana [UNESP]Paula, Verônyca Gonçalves [UNESP]Sinzato, Yuri Karen [UNESP]Damasceno, Débora Cristina [UNESP]Volpato, Gustavo Tadeu2022-04-29T08:32:14Z2022-04-29T08:32:14Z2021-08-10info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.3389/fphys.2021.701767Frontiers in Physiology, v. 12.1664-042Xhttp://hdl.handle.net/11449/22939410.3389/fphys.2021.7017672-s2.0-85113387552Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengFrontiers in Physiologyinfo:eu-repo/semantics/openAccess2024-08-16T14:07:23Zoai:repositorio.unesp.br:11449/229394Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-16T14:07:23Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
title |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
spellingShingle |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats Araujo-Silva, Vanessa Caruline biochemical hyperglycemia malformation obesity pregnancy rat |
title_short |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
title_full |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
title_fullStr |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
title_full_unstemmed |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
title_sort |
Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats |
author |
Araujo-Silva, Vanessa Caruline |
author_facet |
Araujo-Silva, Vanessa Caruline Santos-Silva, Alice Lourenço, Andressa Silva Barros-Barbosa, Cristielly Maria Moraes-Souza, Rafaianne Queiroz [UNESP] Soares, Thaigra Sousa [UNESP] Karki, Barshana [UNESP] Paula, Verônyca Gonçalves [UNESP] Sinzato, Yuri Karen [UNESP] Damasceno, Débora Cristina [UNESP] Volpato, Gustavo Tadeu |
author_role |
author |
author2 |
Santos-Silva, Alice Lourenço, Andressa Silva Barros-Barbosa, Cristielly Maria Moraes-Souza, Rafaianne Queiroz [UNESP] Soares, Thaigra Sousa [UNESP] Karki, Barshana [UNESP] Paula, Verônyca Gonçalves [UNESP] Sinzato, Yuri Karen [UNESP] Damasceno, Débora Cristina [UNESP] Volpato, Gustavo Tadeu |
author2_role |
author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Federal University of Mato Grosso Universidade Estadual Paulista (UNESP) |
dc.contributor.author.fl_str_mv |
Araujo-Silva, Vanessa Caruline Santos-Silva, Alice Lourenço, Andressa Silva Barros-Barbosa, Cristielly Maria Moraes-Souza, Rafaianne Queiroz [UNESP] Soares, Thaigra Sousa [UNESP] Karki, Barshana [UNESP] Paula, Verônyca Gonçalves [UNESP] Sinzato, Yuri Karen [UNESP] Damasceno, Débora Cristina [UNESP] Volpato, Gustavo Tadeu |
dc.subject.por.fl_str_mv |
biochemical hyperglycemia malformation obesity pregnancy rat |
topic |
biochemical hyperglycemia malformation obesity pregnancy rat |
description |
Embryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-08-10 2022-04-29T08:32:14Z 2022-04-29T08:32:14Z |
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/10.3389/fphys.2021.701767 Frontiers in Physiology, v. 12. 1664-042X http://hdl.handle.net/11449/229394 10.3389/fphys.2021.701767 2-s2.0-85113387552 |
url |
http://dx.doi.org/10.3389/fphys.2021.701767 http://hdl.handle.net/11449/229394 |
identifier_str_mv |
Frontiers in Physiology, v. 12. 1664-042X 10.3389/fphys.2021.701767 2-s2.0-85113387552 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Frontiers in Physiology |
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_ |
1808128166949027840 |