Animal models for clinical and gestational diabetes: maternal and fetal outcomes

Detalhes bibliográficos
Autor(a) principal: Kiss, Ana C. I. [UNESP]
Data de Publicação: 2009
Outros Autores: Lima, Paula H. O. [UNESP], Sinzato, Yuri K. [UNESP], Takaku, Mariana [UNESP], Takeno, Marisa A. [UNESP], Rudge, Marilza Vieira Cunha [UNESP], Damasceno, Débora Cristina [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1186/1758-5996-1-21
http://hdl.handle.net/11449/12252
Resumo: Background: Diabetes in pregnant women is associated with an increased risk of maternal and neonatal morbidity and remains a significant medical challenge. Diabetes during pregnancy may be divided into clinical diabetes and gestational diabetes. Experimental models are developed with the purpose of enhancing understanding of the pathophysiological mechanisms of diseases that affect humans. With regard to diabetes in pregnancy, experimental findings from models will lead to the development of treatment strategies to maintain a normal metabolic intrauterine milieu, improving perinatal development by preventing fetal growth restriction or macrosomia. Based on animal models of diabetes during pregnancy previously reported in the medical literature, the present study aimed to compare the impact of streptozotocin-induced severe (glycemia >300 mg/dl) and mild diabetes (glycemia between 120 and 300 mg/dl) on glycemia and maternal reproductive and fetal outcomes of Wistar rats to evaluate whether the animal model reproduces the maternal and perinatal results of clinical and gestational diabetes in humans.Methods: on day 5 of life, 96 female Wistar rats were assigned to three experimental groups: control (n = 16), severe (n = 50) and mild diabetes (n = 30). At day 90 of life, rats were mated. on day 21 of pregnancy, rats were killed and their uterine horns were exposed to count implantation and fetus numbers to determine pre- and post-implantation loss rates. The fetuses were classified according to their birth weight.Results: Severe and mild diabetic dams showed different glycemic responses during pregnancy, impairing fetal glycemia and weight, confirming that maternal glycemia is directly associated with fetal development. Newborns from severe diabetic mothers presented growth restriction, but mild diabetic mothers were not associated with an increased rate of macrosomic fetuses.Conclusion: Experimental models of severe diabetes during pregnancy reproduced maternal and fetal outcomes of pregnant women presenting uncontrolled clinical diabetes. on the other hand, the mild diabetes model caused mild hyperglycemia during pregnancy, although it was not enough to reproduce the increased rate of macrosomic fetuses seen in women with gestational diabetes.
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spelling Animal models for clinical and gestational diabetes: maternal and fetal outcomesBackground: Diabetes in pregnant women is associated with an increased risk of maternal and neonatal morbidity and remains a significant medical challenge. Diabetes during pregnancy may be divided into clinical diabetes and gestational diabetes. Experimental models are developed with the purpose of enhancing understanding of the pathophysiological mechanisms of diseases that affect humans. With regard to diabetes in pregnancy, experimental findings from models will lead to the development of treatment strategies to maintain a normal metabolic intrauterine milieu, improving perinatal development by preventing fetal growth restriction or macrosomia. Based on animal models of diabetes during pregnancy previously reported in the medical literature, the present study aimed to compare the impact of streptozotocin-induced severe (glycemia >300 mg/dl) and mild diabetes (glycemia between 120 and 300 mg/dl) on glycemia and maternal reproductive and fetal outcomes of Wistar rats to evaluate whether the animal model reproduces the maternal and perinatal results of clinical and gestational diabetes in humans.Methods: on day 5 of life, 96 female Wistar rats were assigned to three experimental groups: control (n = 16), severe (n = 50) and mild diabetes (n = 30). At day 90 of life, rats were mated. on day 21 of pregnancy, rats were killed and their uterine horns were exposed to count implantation and fetus numbers to determine pre- and post-implantation loss rates. The fetuses were classified according to their birth weight.Results: Severe and mild diabetic dams showed different glycemic responses during pregnancy, impairing fetal glycemia and weight, confirming that maternal glycemia is directly associated with fetal development. Newborns from severe diabetic mothers presented growth restriction, but mild diabetic mothers were not associated with an increased rate of macrosomic fetuses.Conclusion: Experimental models of severe diabetes during pregnancy reproduced maternal and fetal outcomes of pregnant women presenting uncontrolled clinical diabetes. on the other hand, the mild diabetes model caused mild hyperglycemia during pregnancy, although it was not enough to reproduce the increased rate of macrosomic fetuses seen in women with gestational diabetes.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)São Paulo State Univ Unesp, Botucatu Med Sch, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, São Paulo, BrazilSão Paulo State Univ Unesp, Botucatu Med Sch, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, São Paulo, BrazilBiomed Central Ltd.Universidade Estadual Paulista (Unesp)Kiss, Ana C. I. [UNESP]Lima, Paula H. O. [UNESP]Sinzato, Yuri K. [UNESP]Takaku, Mariana [UNESP]Takeno, Marisa A. [UNESP]Rudge, Marilza Vieira Cunha [UNESP]Damasceno, Débora Cristina [UNESP]2014-05-20T13:35:34Z2014-05-20T13:35:34Z2009-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article7application/pdfhttp://dx.doi.org/10.1186/1758-5996-1-21Diabetology & Metabolic Syndrome. London: Biomed Central Ltd., v. 1, p. 7, 2009.1758-5996http://hdl.handle.net/11449/1225210.1186/1758-5996-1-21WOS:000207918200021WOS000207918200021.pdf67586803888350780000-0002-9227-832XWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengDiabetology & Metabolic Syndrome2.4130,943info:eu-repo/semantics/openAccess2024-08-16T14:07:22Zoai:repositorio.unesp.br:11449/12252Repositório 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 Animal models for clinical and gestational diabetes: maternal and fetal outcomes
title Animal models for clinical and gestational diabetes: maternal and fetal outcomes
spellingShingle Animal models for clinical and gestational diabetes: maternal and fetal outcomes
Kiss, Ana C. I. [UNESP]
title_short Animal models for clinical and gestational diabetes: maternal and fetal outcomes
title_full Animal models for clinical and gestational diabetes: maternal and fetal outcomes
title_fullStr Animal models for clinical and gestational diabetes: maternal and fetal outcomes
title_full_unstemmed Animal models for clinical and gestational diabetes: maternal and fetal outcomes
title_sort Animal models for clinical and gestational diabetes: maternal and fetal outcomes
author Kiss, Ana C. I. [UNESP]
author_facet Kiss, Ana C. I. [UNESP]
Lima, Paula H. O. [UNESP]
Sinzato, Yuri K. [UNESP]
Takaku, Mariana [UNESP]
Takeno, Marisa A. [UNESP]
Rudge, Marilza Vieira Cunha [UNESP]
Damasceno, Débora Cristina [UNESP]
author_role author
author2 Lima, Paula H. O. [UNESP]
Sinzato, Yuri K. [UNESP]
Takaku, Mariana [UNESP]
Takeno, Marisa A. [UNESP]
Rudge, Marilza Vieira Cunha [UNESP]
Damasceno, Débora Cristina [UNESP]
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Kiss, Ana C. I. [UNESP]
Lima, Paula H. O. [UNESP]
Sinzato, Yuri K. [UNESP]
Takaku, Mariana [UNESP]
Takeno, Marisa A. [UNESP]
Rudge, Marilza Vieira Cunha [UNESP]
Damasceno, Débora Cristina [UNESP]
description Background: Diabetes in pregnant women is associated with an increased risk of maternal and neonatal morbidity and remains a significant medical challenge. Diabetes during pregnancy may be divided into clinical diabetes and gestational diabetes. Experimental models are developed with the purpose of enhancing understanding of the pathophysiological mechanisms of diseases that affect humans. With regard to diabetes in pregnancy, experimental findings from models will lead to the development of treatment strategies to maintain a normal metabolic intrauterine milieu, improving perinatal development by preventing fetal growth restriction or macrosomia. Based on animal models of diabetes during pregnancy previously reported in the medical literature, the present study aimed to compare the impact of streptozotocin-induced severe (glycemia >300 mg/dl) and mild diabetes (glycemia between 120 and 300 mg/dl) on glycemia and maternal reproductive and fetal outcomes of Wistar rats to evaluate whether the animal model reproduces the maternal and perinatal results of clinical and gestational diabetes in humans.Methods: on day 5 of life, 96 female Wistar rats were assigned to three experimental groups: control (n = 16), severe (n = 50) and mild diabetes (n = 30). At day 90 of life, rats were mated. on day 21 of pregnancy, rats were killed and their uterine horns were exposed to count implantation and fetus numbers to determine pre- and post-implantation loss rates. The fetuses were classified according to their birth weight.Results: Severe and mild diabetic dams showed different glycemic responses during pregnancy, impairing fetal glycemia and weight, confirming that maternal glycemia is directly associated with fetal development. Newborns from severe diabetic mothers presented growth restriction, but mild diabetic mothers were not associated with an increased rate of macrosomic fetuses.Conclusion: Experimental models of severe diabetes during pregnancy reproduced maternal and fetal outcomes of pregnant women presenting uncontrolled clinical diabetes. on the other hand, the mild diabetes model caused mild hyperglycemia during pregnancy, although it was not enough to reproduce the increased rate of macrosomic fetuses seen in women with gestational diabetes.
publishDate 2009
dc.date.none.fl_str_mv 2009-01-01
2014-05-20T13:35:34Z
2014-05-20T13:35:34Z
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/10.1186/1758-5996-1-21
Diabetology & Metabolic Syndrome. London: Biomed Central Ltd., v. 1, p. 7, 2009.
1758-5996
http://hdl.handle.net/11449/12252
10.1186/1758-5996-1-21
WOS:000207918200021
WOS000207918200021.pdf
6758680388835078
0000-0002-9227-832X
url http://dx.doi.org/10.1186/1758-5996-1-21
http://hdl.handle.net/11449/12252
identifier_str_mv Diabetology & Metabolic Syndrome. London: Biomed Central Ltd., v. 1, p. 7, 2009.
1758-5996
10.1186/1758-5996-1-21
WOS:000207918200021
WOS000207918200021.pdf
6758680388835078
0000-0002-9227-832X
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Diabetology & Metabolic Syndrome
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dc.publisher.none.fl_str_mv Biomed Central Ltd.
publisher.none.fl_str_mv Biomed Central Ltd.
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reponame:Repositório Institucional da UNESP
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