Temporal analysis of distribution pattern of islet cells and antioxidant enzymes for diabetes onset in postnatal critical development window in rats
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , , , , , , |
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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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 |
|
_version_ |
1808128101418270720 |