Pancreatic islet response to diabetes during pregnancy in rats

Detalhes bibliográficos
Autor(a) principal: Gallego, Franciane Quintanilha [UNESP]
Data de Publicação: 2018
Outros Autores: Sinzato, Yuri Karen [UNESP], Miranda, Carolina Abreu [UNESP], Iessi, Isabela Lovizutto [UNESP], Dallaqua, Bruna, Volpato, Gustavo Tadeu, Scarano, Wellerson Rodrigo [UNESP], SanMartín, Sebastian, Damasceno, Débora Cristina [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.lfs.2018.10.046
http://hdl.handle.net/11449/188257
Resumo: Aims: The objective of this study was to assess the mechanisms underlying pancreatic islet adaptation in diabetic mothers and their pups. Additionally, the influence of pancreatic adaptations on maternal reproductive performance was also investigated. Main methods: Wistar rats were injected with streptozotocin for diabetes induction. At adulthood (3 months), all animals underwent an oral glucose tolerance test (OGTT) for glucose assessment as an inclusion criterion. Following, the animals were mated. At day 18 of pregnancy, the mothers were killed for blood collect ion to determine fasting insulin and glucagon concentrations. The pancreas was removed and processed for the immunohistochemical analysis of insulin, glucagon, somatostatin, Ki-67 and PDX-1, superoxide dismutase 1 (SOD-1), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). The pregnant uterus was also collected for the evaluation of embryofetal loss. Key findings: The diabetic rats showed increased glucose, serum glucagon and insulin concentrations, and embryofetal loss rates. They also showed a reduction in pancreatic islets area and percentage of cells stained for insulin, increased the percentage of non-β cells (alpha e delta cells) stained for Ki-67, glucagon, and somatostatin. Moreover, the cells stained for somatostatin were spread across the islets and showed stronger staining for MDA and weaker staining for GSH-Px. Significance: Diabetes leads to adaptive responses from the endocrine pancreas in pregnancy that especially involves non-β cells, modifying the mantle-core structure. Nonetheless, these adaptations are not enough for glucose homeostasis and affect the maternal environment, which in turn impairs fetal development.
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spelling Pancreatic islet response to diabetes during pregnancy in ratsAnimal modelGestationHyperglycemiaPancreasAims: The objective of this study was to assess the mechanisms underlying pancreatic islet adaptation in diabetic mothers and their pups. Additionally, the influence of pancreatic adaptations on maternal reproductive performance was also investigated. Main methods: Wistar rats were injected with streptozotocin for diabetes induction. At adulthood (3 months), all animals underwent an oral glucose tolerance test (OGTT) for glucose assessment as an inclusion criterion. Following, the animals were mated. At day 18 of pregnancy, the mothers were killed for blood collect ion to determine fasting insulin and glucagon concentrations. The pancreas was removed and processed for the immunohistochemical analysis of insulin, glucagon, somatostatin, Ki-67 and PDX-1, superoxide dismutase 1 (SOD-1), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). The pregnant uterus was also collected for the evaluation of embryofetal loss. Key findings: The diabetic rats showed increased glucose, serum glucagon and insulin concentrations, and embryofetal loss rates. They also showed a reduction in pancreatic islets area and percentage of cells stained for insulin, increased the percentage of non-β cells (alpha e delta cells) stained for Ki-67, glucagon, and somatostatin. Moreover, the cells stained for somatostatin were spread across the islets and showed stronger staining for MDA and weaker staining for GSH-Px. Significance: Diabetes leads to adaptive responses from the endocrine pancreas in pregnancy that especially involves non-β cells, modifying the mantle-core structure. Nonetheless, these adaptations are not enough for glucose homeostasis and affect the maternal environment, which in turn impairs fetal development.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Laboratory of Experimental Research on Gynecology and Obstetrics Gynecology Obstetrics and Mastology Post Graduate Course Botucatu Medical School Univ Estadual Paulista_UnespDeVry Ruy Barbosa School (DeVry Brazil Group)Laboratory of System Physiology and Reproductive Toxicology Institute of Biological and Health Sciences Federal University of Mato Grosso (UFMT)Department of Morphology Botucatu Bioscience Institute Univ Estadual Paulista_UnespBiomedical Research Centre Universidad de ValparaísoLaboratory of Experimental Research on Gynecology and Obstetrics Gynecology Obstetrics and Mastology Post Graduate Course Botucatu Medical School Univ Estadual Paulista_UnespDepartment of Morphology Botucatu Bioscience Institute Univ Estadual Paulista_UnespFAPESP: 2011/18519-7Universidade Estadual Paulista (Unesp)DeVry Ruy Barbosa School (DeVry Brazil Group)Federal University of Mato Grosso (UFMT)Universidad de ValparaísoGallego, Franciane Quintanilha [UNESP]Sinzato, Yuri Karen [UNESP]Miranda, Carolina Abreu [UNESP]Iessi, Isabela Lovizutto [UNESP]Dallaqua, BrunaVolpato, Gustavo TadeuScarano, Wellerson Rodrigo [UNESP]SanMartín, SebastianDamasceno, Débora Cristina [UNESP]2019-10-06T16:02:14Z2019-10-06T16:02:14Z2018-12-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1-10http://dx.doi.org/10.1016/j.lfs.2018.10.046Life Sciences, v. 214, p. 1-10.1879-06310024-3205http://hdl.handle.net/11449/18825710.1016/j.lfs.2018.10.0462-s2.0-85055481741Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengLife Sciencesinfo:eu-repo/semantics/openAccess2024-08-16T14:07:22Zoai:repositorio.unesp.br:11449/188257Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-16T14:07:22Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Pancreatic islet response to diabetes during pregnancy in rats
title Pancreatic islet response to diabetes during pregnancy in rats
spellingShingle Pancreatic islet response to diabetes during pregnancy in rats
Gallego, Franciane Quintanilha [UNESP]
Animal model
Gestation
Hyperglycemia
Pancreas
title_short Pancreatic islet response to diabetes during pregnancy in rats
title_full Pancreatic islet response to diabetes during pregnancy in rats
title_fullStr Pancreatic islet response to diabetes during pregnancy in rats
title_full_unstemmed Pancreatic islet response to diabetes during pregnancy in rats
title_sort Pancreatic islet response to diabetes during pregnancy in rats
author Gallego, Franciane Quintanilha [UNESP]
author_facet Gallego, Franciane Quintanilha [UNESP]
Sinzato, Yuri Karen [UNESP]
Miranda, Carolina Abreu [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Volpato, Gustavo Tadeu
Scarano, Wellerson Rodrigo [UNESP]
SanMartín, Sebastian
Damasceno, Débora Cristina [UNESP]
author_role author
author2 Sinzato, Yuri Karen [UNESP]
Miranda, Carolina Abreu [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Volpato, Gustavo Tadeu
Scarano, Wellerson Rodrigo [UNESP]
SanMartín, Sebastian
Damasceno, Débora Cristina [UNESP]
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
DeVry Ruy Barbosa School (DeVry Brazil Group)
Federal University of Mato Grosso (UFMT)
Universidad de Valparaíso
dc.contributor.author.fl_str_mv Gallego, Franciane Quintanilha [UNESP]
Sinzato, Yuri Karen [UNESP]
Miranda, Carolina Abreu [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Volpato, Gustavo Tadeu
Scarano, Wellerson Rodrigo [UNESP]
SanMartín, Sebastian
Damasceno, Débora Cristina [UNESP]
dc.subject.por.fl_str_mv Animal model
Gestation
Hyperglycemia
Pancreas
topic Animal model
Gestation
Hyperglycemia
Pancreas
description Aims: The objective of this study was to assess the mechanisms underlying pancreatic islet adaptation in diabetic mothers and their pups. Additionally, the influence of pancreatic adaptations on maternal reproductive performance was also investigated. Main methods: Wistar rats were injected with streptozotocin for diabetes induction. At adulthood (3 months), all animals underwent an oral glucose tolerance test (OGTT) for glucose assessment as an inclusion criterion. Following, the animals were mated. At day 18 of pregnancy, the mothers were killed for blood collect ion to determine fasting insulin and glucagon concentrations. The pancreas was removed and processed for the immunohistochemical analysis of insulin, glucagon, somatostatin, Ki-67 and PDX-1, superoxide dismutase 1 (SOD-1), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). The pregnant uterus was also collected for the evaluation of embryofetal loss. Key findings: The diabetic rats showed increased glucose, serum glucagon and insulin concentrations, and embryofetal loss rates. They also showed a reduction in pancreatic islets area and percentage of cells stained for insulin, increased the percentage of non-β cells (alpha e delta cells) stained for Ki-67, glucagon, and somatostatin. Moreover, the cells stained for somatostatin were spread across the islets and showed stronger staining for MDA and weaker staining for GSH-Px. Significance: Diabetes leads to adaptive responses from the endocrine pancreas in pregnancy that especially involves non-β cells, modifying the mantle-core structure. Nonetheless, these adaptations are not enough for glucose homeostasis and affect the maternal environment, which in turn impairs fetal development.
publishDate 2018
dc.date.none.fl_str_mv 2018-12-01
2019-10-06T16:02:14Z
2019-10-06T16:02:14Z
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/10.1016/j.lfs.2018.10.046
Life Sciences, v. 214, p. 1-10.
1879-0631
0024-3205
http://hdl.handle.net/11449/188257
10.1016/j.lfs.2018.10.046
2-s2.0-85055481741
url http://dx.doi.org/10.1016/j.lfs.2018.10.046
http://hdl.handle.net/11449/188257
identifier_str_mv Life Sciences, v. 214, p. 1-10.
1879-0631
0024-3205
10.1016/j.lfs.2018.10.046
2-s2.0-85055481741
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Life Sciences
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1-10
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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