Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.3389/fcell.2022.818621 http://hdl.handle.net/11449/241181 |
Resumo: | Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy. |
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Maternal Diabetes and Postnatal High-Fat Diet on Pregnant OffspringdiabetesFemale reproductionfetal programmingmalnutritionrodentMaternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Laboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Course on Tocogynecology Botucatu Medical School Sao Paulo State University (UNESP)Research Support Office Botucatu Medical School Sao Paulo State University (UNESP)Laboratory of System Physiology and Reproductive Toxicology Institute of Biological and Health Sciences Federal University of Mato Grosso (UFMT)Laboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Course on Tocogynecology Botucatu Medical School Sao Paulo State University (UNESP)Research Support Office Botucatu Medical School Sao Paulo State University (UNESP)Universidade Estadual Paulista (UNESP)Federal University of Mato Grosso (UFMT)Sinzato, Yuri Karen [UNESP]Paula, Verônyca Gonçalves [UNESP]Gallego, Franciane Quintanilha [UNESP]Moraes-Souza, Rafaianne Q. [UNESP]Corrente, José Eduardo [UNESP]Volpato, Gustavo TadeuDamasceno, Débora Cristina [UNESP]2023-03-01T20:50:36Z2023-03-01T20:50:36Z2022-05-30info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.3389/fcell.2022.818621Frontiers in Cell and Developmental Biology, v. 10.2296-634Xhttp://hdl.handle.net/11449/24118110.3389/fcell.2022.8186212-s2.0-85132243130Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengFrontiers in Cell and Developmental Biologyinfo:eu-repo/semantics/openAccess2023-03-01T20:50:36Zoai:repositorio.unesp.br:11449/241181Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462023-03-01T20:50:36Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
title |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
spellingShingle |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring Sinzato, Yuri Karen [UNESP] diabetes Female reproduction fetal programming malnutrition rodent |
title_short |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
title_full |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
title_fullStr |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
title_full_unstemmed |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
title_sort |
Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring |
author |
Sinzato, Yuri Karen [UNESP] |
author_facet |
Sinzato, Yuri Karen [UNESP] Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Moraes-Souza, Rafaianne Q. [UNESP] Corrente, José Eduardo [UNESP] Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
author_role |
author |
author2 |
Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Moraes-Souza, Rafaianne Q. [UNESP] Corrente, José Eduardo [UNESP] Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (UNESP) Federal University of Mato Grosso (UFMT) |
dc.contributor.author.fl_str_mv |
Sinzato, Yuri Karen [UNESP] Paula, Verônyca Gonçalves [UNESP] Gallego, Franciane Quintanilha [UNESP] Moraes-Souza, Rafaianne Q. [UNESP] Corrente, José Eduardo [UNESP] Volpato, Gustavo Tadeu Damasceno, Débora Cristina [UNESP] |
dc.subject.por.fl_str_mv |
diabetes Female reproduction fetal programming malnutrition rodent |
topic |
diabetes Female reproduction fetal programming malnutrition rodent |
description |
Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-05-30 2023-03-01T20:50:36Z 2023-03-01T20:50:36Z |
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/fcell.2022.818621 Frontiers in Cell and Developmental Biology, v. 10. 2296-634X http://hdl.handle.net/11449/241181 10.3389/fcell.2022.818621 2-s2.0-85132243130 |
url |
http://dx.doi.org/10.3389/fcell.2022.818621 http://hdl.handle.net/11449/241181 |
identifier_str_mv |
Frontiers in Cell and Developmental Biology, v. 10. 2296-634X 10.3389/fcell.2022.818621 2-s2.0-85132243130 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Frontiers in Cell and Developmental Biology |
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 |
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1803046385567662080 |