Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1093/biolre/ioab195 http://hdl.handle.net/11449/218771 |
Resumo: | We evaluated the influence of the hyperglycemic intrauterine environment and postweaning consumption of a high-fat diet (HFD) on the glycemia, insulin, lipid, and immunological profile of rat offspring in adulthood. Female rats received citrate buffer (Control-C) or Streptozotocin (a beta cell-cytotoxic drug to induce diabetes-D) on postnatal day 5. In adulthood, these rats were mated to obtain female offspring, who were fed a standard diet (SD) or HFD from weaning to adulthood (n = 10 rats/group). OC/SD and OC/HFD represent female offspring of control mothers and received SD or HFD, respectively; OD/SD and OD/HFD represent female offspring of diabetic mothers and received SD or HFD, respectively. At adulthood, the oral glucose tolerance test (OGTT) was performed and, next, the rats were anesthetized and euthanized. Pancreas was collected and analyzed, and adipose tissue was weighted. Blood samples were collected to determine biochemical and immunological profiles. The food intake was lower in HFD-fed rats and visceral fat weight was increased in the OD/HFD group. OC/HFD, OD/SD, and OD/HFD groups presented glucose intolerance and lower insulin secretion during OGTT. An impaired pancreatic beta-cell function was shown in the adult offspring of diabetic rats, regardless of diet. Interleukin (IL)-6 and IL-10 concentrations were lower in the OD/HFD group and associated to a low-grade inflammatory condition. The fetal programming was responsible for impaired beta cell function in experimental animals. The association of maternal diabetes and postweaning HFD are responsible for greater glucose intolerance, impaired insulin secretion and immunological change. Summary sentence Summary Sentence The association of maternal diabetes and postweaning HFD causes glucose intolerance due to beta-cell disarrangement and impaired insulin secretion, and immunological changes in adult offspring. |
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Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat dietfetal programminghigh-fat dietdiabetesratWe evaluated the influence of the hyperglycemic intrauterine environment and postweaning consumption of a high-fat diet (HFD) on the glycemia, insulin, lipid, and immunological profile of rat offspring in adulthood. Female rats received citrate buffer (Control-C) or Streptozotocin (a beta cell-cytotoxic drug to induce diabetes-D) on postnatal day 5. In adulthood, these rats were mated to obtain female offspring, who were fed a standard diet (SD) or HFD from weaning to adulthood (n = 10 rats/group). OC/SD and OC/HFD represent female offspring of control mothers and received SD or HFD, respectively; OD/SD and OD/HFD represent female offspring of diabetic mothers and received SD or HFD, respectively. At adulthood, the oral glucose tolerance test (OGTT) was performed and, next, the rats were anesthetized and euthanized. Pancreas was collected and analyzed, and adipose tissue was weighted. Blood samples were collected to determine biochemical and immunological profiles. The food intake was lower in HFD-fed rats and visceral fat weight was increased in the OD/HFD group. OC/HFD, OD/SD, and OD/HFD groups presented glucose intolerance and lower insulin secretion during OGTT. An impaired pancreatic beta-cell function was shown in the adult offspring of diabetic rats, regardless of diet. Interleukin (IL)-6 and IL-10 concentrations were lower in the OD/HFD group and associated to a low-grade inflammatory condition. The fetal programming was responsible for impaired beta cell function in experimental animals. The association of maternal diabetes and postweaning HFD are responsible for greater glucose intolerance, impaired insulin secretion and immunological change. Summary sentence Summary Sentence The association of maternal diabetes and postweaning HFD causes glucose intolerance due to beta-cell disarrangement and impaired insulin secretion, and immunological changes in adult offspring.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)SJo Paulo State Univ UNESP, Botucatu Med Sch, Lab Expt Res Gynecol & Obstet, Tocogynecol Postgrad Course, Botucatu, SP, BrazilFed Univ Mato Grosso UFMT, Inst Biol & Hlth Sci, Lab Syst Physiol & Reprod Toxicol, Barra Do Garcas, MT, BrazilFed Univ Maranhao UFMA, Dept Physiol Sci, Lab Expt Physiol, Sao Luis, MA, BrazilUniv Estadual Paulista UNESP, Botucatu Med Sch, Res Support Off, Botucatu, SP, BrazilSJo Paulo State Univ UNESP, Botucatu Med Sch, Lab Expt Res Gynecol & Obstet, Tocogynecol Postgrad Course, Botucatu, SP, BrazilUniv Estadual Paulista UNESP, Botucatu Med Sch, Res Support Off, Botucatu, SP, BrazilFAPESP: 2016/25207-5Oxford Univ Press IncUniversidade Estadual Paulista (UNESP)Universidade Federal de Mato Grosso do Sul (UFMS)Fed Univ Maranhao UFMAPaula, Veronyca Goncalves [UNESP]Sinzato, Yuri Karen [UNESP]Moraes-Souza, Rafaianne Queiroz de [UNESP]Soares, Thaigra Sousa [UNESP]Gallego Souza, Franciane Quintanilha [UNESP]Karki, Barshana [UNESP]Andrade Paes, Antonio Marcus deCorrente, Jose Eduardo [UNESP]Damasceno, Debora Cristina [UNESP]Volpato, Gustavo Tadeu2022-04-28T17:22:59Z2022-04-28T17:22:59Z2021-10-20info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article200-212http://dx.doi.org/10.1093/biolre/ioab195Biology Of Reproduction. Cary: Oxford Univ Press Inc, v. 106, n. 1, p. 200-212, 2022.0006-3363http://hdl.handle.net/11449/21877110.1093/biolre/ioab195WOS:000743464500018Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengBiology Of Reproductioninfo:eu-repo/semantics/openAccess2024-08-16T14:06:23Zoai:repositorio.unesp.br:11449/218771Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-16T14:06:23Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
title |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
spellingShingle |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet Paula, Veronyca Goncalves [UNESP] fetal programming high-fat diet diabetes rat |
title_short |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
title_full |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
title_fullStr |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
title_full_unstemmed |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
title_sort |
Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet |
author |
Paula, Veronyca Goncalves [UNESP] |
author_facet |
Paula, Veronyca Goncalves [UNESP] Sinzato, Yuri Karen [UNESP] Moraes-Souza, Rafaianne Queiroz de [UNESP] Soares, Thaigra Sousa [UNESP] Gallego Souza, Franciane Quintanilha [UNESP] Karki, Barshana [UNESP] Andrade Paes, Antonio Marcus de Corrente, Jose Eduardo [UNESP] Damasceno, Debora Cristina [UNESP] Volpato, Gustavo Tadeu |
author_role |
author |
author2 |
Sinzato, Yuri Karen [UNESP] Moraes-Souza, Rafaianne Queiroz de [UNESP] Soares, Thaigra Sousa [UNESP] Gallego Souza, Franciane Quintanilha [UNESP] Karki, Barshana [UNESP] Andrade Paes, Antonio Marcus de Corrente, Jose Eduardo [UNESP] Damasceno, Debora Cristina [UNESP] Volpato, Gustavo Tadeu |
author2_role |
author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (UNESP) Universidade Federal de Mato Grosso do Sul (UFMS) Fed Univ Maranhao UFMA |
dc.contributor.author.fl_str_mv |
Paula, Veronyca Goncalves [UNESP] Sinzato, Yuri Karen [UNESP] Moraes-Souza, Rafaianne Queiroz de [UNESP] Soares, Thaigra Sousa [UNESP] Gallego Souza, Franciane Quintanilha [UNESP] Karki, Barshana [UNESP] Andrade Paes, Antonio Marcus de Corrente, Jose Eduardo [UNESP] Damasceno, Debora Cristina [UNESP] Volpato, Gustavo Tadeu |
dc.subject.por.fl_str_mv |
fetal programming high-fat diet diabetes rat |
topic |
fetal programming high-fat diet diabetes rat |
description |
We evaluated the influence of the hyperglycemic intrauterine environment and postweaning consumption of a high-fat diet (HFD) on the glycemia, insulin, lipid, and immunological profile of rat offspring in adulthood. Female rats received citrate buffer (Control-C) or Streptozotocin (a beta cell-cytotoxic drug to induce diabetes-D) on postnatal day 5. In adulthood, these rats were mated to obtain female offspring, who were fed a standard diet (SD) or HFD from weaning to adulthood (n = 10 rats/group). OC/SD and OC/HFD represent female offspring of control mothers and received SD or HFD, respectively; OD/SD and OD/HFD represent female offspring of diabetic mothers and received SD or HFD, respectively. At adulthood, the oral glucose tolerance test (OGTT) was performed and, next, the rats were anesthetized and euthanized. Pancreas was collected and analyzed, and adipose tissue was weighted. Blood samples were collected to determine biochemical and immunological profiles. The food intake was lower in HFD-fed rats and visceral fat weight was increased in the OD/HFD group. OC/HFD, OD/SD, and OD/HFD groups presented glucose intolerance and lower insulin secretion during OGTT. An impaired pancreatic beta-cell function was shown in the adult offspring of diabetic rats, regardless of diet. Interleukin (IL)-6 and IL-10 concentrations were lower in the OD/HFD group and associated to a low-grade inflammatory condition. The fetal programming was responsible for impaired beta cell function in experimental animals. The association of maternal diabetes and postweaning HFD are responsible for greater glucose intolerance, impaired insulin secretion and immunological change. Summary sentence Summary Sentence The association of maternal diabetes and postweaning HFD causes glucose intolerance due to beta-cell disarrangement and impaired insulin secretion, and immunological changes in adult offspring. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-10-20 2022-04-28T17:22:59Z 2022-04-28T17:22:59Z |
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/10.1093/biolre/ioab195 Biology Of Reproduction. Cary: Oxford Univ Press Inc, v. 106, n. 1, p. 200-212, 2022. 0006-3363 http://hdl.handle.net/11449/218771 10.1093/biolre/ioab195 WOS:000743464500018 |
url |
http://dx.doi.org/10.1093/biolre/ioab195 http://hdl.handle.net/11449/218771 |
identifier_str_mv |
Biology Of Reproduction. Cary: Oxford Univ Press Inc, v. 106, n. 1, p. 200-212, 2022. 0006-3363 10.1093/biolre/ioab195 WOS:000743464500018 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Biology Of Reproduction |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
200-212 |
dc.publisher.none.fl_str_mv |
Oxford Univ Press Inc |
publisher.none.fl_str_mv |
Oxford Univ Press Inc |
dc.source.none.fl_str_mv |
Web of Science 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_ |
1808128103570997248 |