Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats

Detalhes bibliográficos
Autor(a) principal: Gallego, Franciane Quintanilha [UNESP]
Data de Publicação: 2019
Outros Autores: Miranda, Carolina Abreu [UNESP], Sinzato, Yuri Karen [UNESP], Iessi, Isabela Lovizutto [UNESP], Dallaqua, Bruna, Pando, Rogelio Hernandez, Rocha, Noeme Sousa [UNESP], Volpato, Gustavo Tadeu, 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.2019.03.061
http://hdl.handle.net/11449/188973
Resumo: Aim: At performing a temporal analysis of the distribution pattern of islet endocrine cells and antioxidant enzymes in diabetic rats during the post-natal critical development window. Main methods: The newborns received streptozotocin (STZ) at birth for diabetes induction, and control females received the vehicle. The animals were euthanized at different lifetimes: D5, D10, D15, and D30. Morphological analysis of pancreas and biochemical assays was performed. Key findings: The STZ-induced rats presented irregular shape of islet on D5 and there was an attempt to restore of this shape in other life moment studied. There was an increase progressive in islet area, however they maintained smaller than those of control rats, with lower labeling intensity for insulin, higher for glucagon and somatostatin, lower for SOD-1 was lower in the islets of the STZ-induced animals at all times studied and for GSH-Px in D10 and D30. Significance: Although STZ-induced diabetic rats presented compensatory mechanisms to restore the mass of endocrine cells, this was not sufficient since these rats developed the diabetic state. This was confirmed by the oral glucose tolerance test from D30. In addition, the delta (δ)-cells presented ectopic location in islets, indicating a possible relationship for beta (β)-cell mass restoration. There was a response of the pancreas to reduce the hyperglycemia in the first month of life. Furthermore, the cells from the endocrine pancreas of diabetic animals show a decline of antioxidant enzymatic, contributing to the increased susceptibility of cells to hyperglycemia-induced ROS in this postnatal critical development window.
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spelling Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in ratsGlucagonInsulinOxidative stressRatsSomatostatinAim: At performing a temporal analysis of the distribution pattern of islet endocrine cells and antioxidant enzymes in diabetic rats during the post-natal critical development window. Main methods: The newborns received streptozotocin (STZ) at birth for diabetes induction, and control females received the vehicle. The animals were euthanized at different lifetimes: D5, D10, D15, and D30. Morphological analysis of pancreas and biochemical assays was performed. Key findings: The STZ-induced rats presented irregular shape of islet on D5 and there was an attempt to restore of this shape in other life moment studied. There was an increase progressive in islet area, however they maintained smaller than those of control rats, with lower labeling intensity for insulin, higher for glucagon and somatostatin, lower for SOD-1 was lower in the islets of the STZ-induced animals at all times studied and for GSH-Px in D10 and D30. Significance: Although STZ-induced diabetic rats presented compensatory mechanisms to restore the mass of endocrine cells, this was not sufficient since these rats developed the diabetic state. This was confirmed by the oral glucose tolerance test from D30. In addition, the delta (δ)-cells presented ectopic location in islets, indicating a possible relationship for beta (β)-cell mass restoration. There was a response of the pancreas to reduce the hyperglycemia in the first month of life. Furthermore, the cells from the endocrine pancreas of diabetic animals show a decline of antioxidant enzymatic, contributing to the increased susceptibility of cells to hyperglycemia-induced ROS in this postnatal critical development window.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Laboratory of Experimental Research of Gynecology and Obstetrics Postgraduate Course of Gynecology Obstetrics and Mastology Botucatu Medical School São Paulo State University (UNESP)DeVry Ruy Barbosa School (DeVry Brazil Group)Department of Pathology National Institute of Medical Sciences and Nutrition “Salvador Zubirán”Department of Pathology School of Veterinary Medicine and Animal Science (FMVZ) São 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 of Gynecology and Obstetrics Postgraduate Course of Gynecology Obstetrics and Mastology Botucatu Medical School São Paulo State University (UNESP)Department of Pathology School of Veterinary Medicine and Animal Science (FMVZ) São Paulo State University (UNESP)FAPESP: 2011/18519-7Universidade Estadual Paulista (Unesp)DeVry Ruy Barbosa School (DeVry Brazil Group)National Institute of Medical Sciences and Nutrition “Salvador Zubirán”Federal University of Mato Grosso (UFMT)Gallego, Franciane Quintanilha [UNESP]Miranda, Carolina Abreu [UNESP]Sinzato, Yuri Karen [UNESP]Iessi, Isabela Lovizutto [UNESP]Dallaqua, BrunaPando, Rogelio HernandezRocha, Noeme Sousa [UNESP]Volpato, Gustavo TadeuDamasceno, Débora Cristina [UNESP]2019-10-06T16:25:39Z2019-10-06T16:25:39Z2019-06-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article57-67http://dx.doi.org/10.1016/j.lfs.2019.03.061Life Sciences, v. 226, p. 57-67.1879-06310024-3205http://hdl.handle.net/11449/18897310.1016/j.lfs.2019.03.0612-s2.0-8506425144260777359184692840000-0002-8188-8149Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengLife Sciencesinfo:eu-repo/semantics/openAccess2024-08-16T14:06:22Zoai:repositorio.unesp.br:11449/188973Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-16T14:06:22Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
title Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
spellingShingle Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
Gallego, Franciane Quintanilha [UNESP]
Glucagon
Insulin
Oxidative stress
Rats
Somatostatin
title_short Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
title_full Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
title_fullStr Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
title_full_unstemmed Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
title_sort Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
author Gallego, Franciane Quintanilha [UNESP]
author_facet Gallego, Franciane Quintanilha [UNESP]
Miranda, Carolina Abreu [UNESP]
Sinzato, Yuri Karen [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Pando, Rogelio Hernandez
Rocha, Noeme Sousa [UNESP]
Volpato, Gustavo Tadeu
Damasceno, Débora Cristina [UNESP]
author_role author
author2 Miranda, Carolina Abreu [UNESP]
Sinzato, Yuri Karen [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Pando, Rogelio Hernandez
Rocha, Noeme Sousa [UNESP]
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)
DeVry Ruy Barbosa School (DeVry Brazil Group)
National Institute of Medical Sciences and Nutrition “Salvador Zubirán”
Federal University of Mato Grosso (UFMT)
dc.contributor.author.fl_str_mv Gallego, Franciane Quintanilha [UNESP]
Miranda, Carolina Abreu [UNESP]
Sinzato, Yuri Karen [UNESP]
Iessi, Isabela Lovizutto [UNESP]
Dallaqua, Bruna
Pando, Rogelio Hernandez
Rocha, Noeme Sousa [UNESP]
Volpato, Gustavo Tadeu
Damasceno, Débora Cristina [UNESP]
dc.subject.por.fl_str_mv Glucagon
Insulin
Oxidative stress
Rats
Somatostatin
topic Glucagon
Insulin
Oxidative stress
Rats
Somatostatin
description Aim: At performing a temporal analysis of the distribution pattern of islet endocrine cells and antioxidant enzymes in diabetic rats during the post-natal critical development window. Main methods: The newborns received streptozotocin (STZ) at birth for diabetes induction, and control females received the vehicle. The animals were euthanized at different lifetimes: D5, D10, D15, and D30. Morphological analysis of pancreas and biochemical assays was performed. Key findings: The STZ-induced rats presented irregular shape of islet on D5 and there was an attempt to restore of this shape in other life moment studied. There was an increase progressive in islet area, however they maintained smaller than those of control rats, with lower labeling intensity for insulin, higher for glucagon and somatostatin, lower for SOD-1 was lower in the islets of the STZ-induced animals at all times studied and for GSH-Px in D10 and D30. Significance: Although STZ-induced diabetic rats presented compensatory mechanisms to restore the mass of endocrine cells, this was not sufficient since these rats developed the diabetic state. This was confirmed by the oral glucose tolerance test from D30. In addition, the delta (δ)-cells presented ectopic location in islets, indicating a possible relationship for beta (β)-cell mass restoration. There was a response of the pancreas to reduce the hyperglycemia in the first month of life. Furthermore, the cells from the endocrine pancreas of diabetic animals show a decline of antioxidant enzymatic, contributing to the increased susceptibility of cells to hyperglycemia-induced ROS in this postnatal critical development window.
publishDate 2019
dc.date.none.fl_str_mv 2019-10-06T16:25:39Z
2019-10-06T16:25:39Z
2019-06-01
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/10.1016/j.lfs.2019.03.061
Life Sciences, v. 226, p. 57-67.
1879-0631
0024-3205
http://hdl.handle.net/11449/188973
10.1016/j.lfs.2019.03.061
2-s2.0-85064251442
6077735918469284
0000-0002-8188-8149
url http://dx.doi.org/10.1016/j.lfs.2019.03.061
http://hdl.handle.net/11449/188973
identifier_str_mv Life Sciences, v. 226, p. 57-67.
1879-0631
0024-3205
10.1016/j.lfs.2019.03.061
2-s2.0-85064251442
6077735918469284
0000-0002-8188-8149
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 57-67
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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