Sitagliptin protects proliferation of neural progenitor cells in diabetic mice

Autores
Bachor, Tomás Pedro; Marquioni Ramella, Melisa Daniela; Suburo, Angela Maria
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Sitagliptin (SIT) is a dipeptidyl peptidase-4 (DPP-4) inhibitor that enhances the effects of incretin hormones, such as Glucose-dependent Insulinotropic Peptide (also known as Gastric Inhibitory Polypeptide, GIP) and Glucagon-Like Peptide 1 (GLP-1). We have now evaluated the effect of SIT on proliferation of neural progenitors in diabetic mice. A condition resembling the non-obese type 2 diabetes mellitus (D2) was achieved by a combination of streptozotocin and nicotinamide (NA-STZ), whereas a type 1-like disease (D1) was provoked by STZ without NA. Nondiabetic mice received vehicle injections. Cell proliferation was estimated by bromodeoxyuridine (BrdU) incorporation in two different regions of the subventricular zone (SVZ), the largest reserve of neural stem cells in the adult brain. SIT treatment did not modify the high fasting blood glucose (BG) levels and intraperitoneal glucose tolerance test (IPGTT) of D1 mice. By contrast, in D2 mice, SIT treatment significantly reduced BG and IPGTT. Both D1 and D2 mice showed a substantial reduction of BrdU labeling in the SVZ. Remarkably, SIT treatment improved BrdU labeling in both conditions. Our findings suggest that SIT would protect proliferation of neural progenitor cells even in the presence of non-controlled diabetic alterations.
Fil: Bachor, Tomás Pedro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina
Fil: Marquioni Ramella, Melisa Daniela. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Suburo, Angela Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
DIABETES
GLIPTINS
GLUCAGON-LIKE PEPTIDE 1
NEURAL STEM CELLS
NEUROGENESIS
SUBVENTRICULAR ZONE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/99196

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network_name_str CONICET Digital (CONICET)
spelling Sitagliptin protects proliferation of neural progenitor cells in diabetic miceBachor, Tomás PedroMarquioni Ramella, Melisa DanielaSuburo, Angela MariaDIABETESGLIPTINSGLUCAGON-LIKE PEPTIDE 1NEURAL STEM CELLSNEUROGENESISSUBVENTRICULAR ZONEhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Sitagliptin (SIT) is a dipeptidyl peptidase-4 (DPP-4) inhibitor that enhances the effects of incretin hormones, such as Glucose-dependent Insulinotropic Peptide (also known as Gastric Inhibitory Polypeptide, GIP) and Glucagon-Like Peptide 1 (GLP-1). We have now evaluated the effect of SIT on proliferation of neural progenitors in diabetic mice. A condition resembling the non-obese type 2 diabetes mellitus (D2) was achieved by a combination of streptozotocin and nicotinamide (NA-STZ), whereas a type 1-like disease (D1) was provoked by STZ without NA. Nondiabetic mice received vehicle injections. Cell proliferation was estimated by bromodeoxyuridine (BrdU) incorporation in two different regions of the subventricular zone (SVZ), the largest reserve of neural stem cells in the adult brain. SIT treatment did not modify the high fasting blood glucose (BG) levels and intraperitoneal glucose tolerance test (IPGTT) of D1 mice. By contrast, in D2 mice, SIT treatment significantly reduced BG and IPGTT. Both D1 and D2 mice showed a substantial reduction of BrdU labeling in the SVZ. Remarkably, SIT treatment improved BrdU labeling in both conditions. Our findings suggest that SIT would protect proliferation of neural progenitor cells even in the presence of non-controlled diabetic alterations.Fil: Bachor, Tomás Pedro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; ArgentinaFil: Marquioni Ramella, Melisa Daniela. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Suburo, Angela Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaSpringer/Plenum Publishers2015-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/99196Bachor, Tomás Pedro; Marquioni Ramella, Melisa Daniela; Suburo, Angela Maria; Sitagliptin protects proliferation of neural progenitor cells in diabetic mice; Springer/Plenum Publishers; Metabolic Brain Disease; 30; 4; 8-2015; 885-8930885-7490CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11011-015-9656-2info:eu-repo/semantics/altIdentifier/doi/10.1007/s11011-015-9656-2info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:32:34Zoai:ri.conicet.gov.ar:11336/99196instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:32:34.315CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
title Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
spellingShingle Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
Bachor, Tomás Pedro
DIABETES
GLIPTINS
GLUCAGON-LIKE PEPTIDE 1
NEURAL STEM CELLS
NEUROGENESIS
SUBVENTRICULAR ZONE
title_short Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
title_full Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
title_fullStr Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
title_full_unstemmed Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
title_sort Sitagliptin protects proliferation of neural progenitor cells in diabetic mice
dc.creator.none.fl_str_mv Bachor, Tomás Pedro
Marquioni Ramella, Melisa Daniela
Suburo, Angela Maria
author Bachor, Tomás Pedro
author_facet Bachor, Tomás Pedro
Marquioni Ramella, Melisa Daniela
Suburo, Angela Maria
author_role author
author2 Marquioni Ramella, Melisa Daniela
Suburo, Angela Maria
author2_role author
author
dc.subject.none.fl_str_mv DIABETES
GLIPTINS
GLUCAGON-LIKE PEPTIDE 1
NEURAL STEM CELLS
NEUROGENESIS
SUBVENTRICULAR ZONE
topic DIABETES
GLIPTINS
GLUCAGON-LIKE PEPTIDE 1
NEURAL STEM CELLS
NEUROGENESIS
SUBVENTRICULAR ZONE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Sitagliptin (SIT) is a dipeptidyl peptidase-4 (DPP-4) inhibitor that enhances the effects of incretin hormones, such as Glucose-dependent Insulinotropic Peptide (also known as Gastric Inhibitory Polypeptide, GIP) and Glucagon-Like Peptide 1 (GLP-1). We have now evaluated the effect of SIT on proliferation of neural progenitors in diabetic mice. A condition resembling the non-obese type 2 diabetes mellitus (D2) was achieved by a combination of streptozotocin and nicotinamide (NA-STZ), whereas a type 1-like disease (D1) was provoked by STZ without NA. Nondiabetic mice received vehicle injections. Cell proliferation was estimated by bromodeoxyuridine (BrdU) incorporation in two different regions of the subventricular zone (SVZ), the largest reserve of neural stem cells in the adult brain. SIT treatment did not modify the high fasting blood glucose (BG) levels and intraperitoneal glucose tolerance test (IPGTT) of D1 mice. By contrast, in D2 mice, SIT treatment significantly reduced BG and IPGTT. Both D1 and D2 mice showed a substantial reduction of BrdU labeling in the SVZ. Remarkably, SIT treatment improved BrdU labeling in both conditions. Our findings suggest that SIT would protect proliferation of neural progenitor cells even in the presence of non-controlled diabetic alterations.
Fil: Bachor, Tomás Pedro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina
Fil: Marquioni Ramella, Melisa Daniela. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Suburo, Angela Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description Sitagliptin (SIT) is a dipeptidyl peptidase-4 (DPP-4) inhibitor that enhances the effects of incretin hormones, such as Glucose-dependent Insulinotropic Peptide (also known as Gastric Inhibitory Polypeptide, GIP) and Glucagon-Like Peptide 1 (GLP-1). We have now evaluated the effect of SIT on proliferation of neural progenitors in diabetic mice. A condition resembling the non-obese type 2 diabetes mellitus (D2) was achieved by a combination of streptozotocin and nicotinamide (NA-STZ), whereas a type 1-like disease (D1) was provoked by STZ without NA. Nondiabetic mice received vehicle injections. Cell proliferation was estimated by bromodeoxyuridine (BrdU) incorporation in two different regions of the subventricular zone (SVZ), the largest reserve of neural stem cells in the adult brain. SIT treatment did not modify the high fasting blood glucose (BG) levels and intraperitoneal glucose tolerance test (IPGTT) of D1 mice. By contrast, in D2 mice, SIT treatment significantly reduced BG and IPGTT. Both D1 and D2 mice showed a substantial reduction of BrdU labeling in the SVZ. Remarkably, SIT treatment improved BrdU labeling in both conditions. Our findings suggest that SIT would protect proliferation of neural progenitor cells even in the presence of non-controlled diabetic alterations.
publishDate 2015
dc.date.none.fl_str_mv 2015-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/99196
Bachor, Tomás Pedro; Marquioni Ramella, Melisa Daniela; Suburo, Angela Maria; Sitagliptin protects proliferation of neural progenitor cells in diabetic mice; Springer/Plenum Publishers; Metabolic Brain Disease; 30; 4; 8-2015; 885-893
0885-7490
CONICET Digital
CONICET
url http://hdl.handle.net/11336/99196
identifier_str_mv Bachor, Tomás Pedro; Marquioni Ramella, Melisa Daniela; Suburo, Angela Maria; Sitagliptin protects proliferation of neural progenitor cells in diabetic mice; Springer/Plenum Publishers; Metabolic Brain Disease; 30; 4; 8-2015; 885-893
0885-7490
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11011-015-9656-2
info:eu-repo/semantics/altIdentifier/doi/10.1007/s11011-015-9656-2
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer/Plenum Publishers
publisher.none.fl_str_mv Springer/Plenum Publishers
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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