VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins
- Autores
- Maiztegui, Barbara; Boggio, Veronica; Román, Carolina Lisi; Flores, Luis Emilio; del Zotto, Hector Herminio; Ropolo, Alejandro Javier; Grasso, Daniel Hector; Vaccaro, Maria Ines; Gagliardino, Juan Jose
- Año de publicación
- 2017
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The aim of the present study was to demonstrate the role of autophagy and incretins inthe fructose-induced alteration of β-cell mass and function. Normal Wistar rats were fed(3 weeks) with a commercial diet without (C) or with 10% fructose in drinking water (F) aloneor plus sitagliptin (CS and FS) or exendin-4 (CE and FE). Serum levels of metabolic/endocrineparameters, B-cell mass, morphology/ultrastructure and apoptosis, vacuole membrane protein1 (VMP1) expression and glucose-stimulated insulin secretion (GSIS) were studied.Complementary to this, islets isolated from normal rats were cultured (3 days) without (C) orwith F and F + exendin-4 or chloroquine. Expression of autophagy-related proteins [VMP1and microtubule-associated protein light chain 3 (LC3)], apoptotic/antiapoptotic markers(caspase-3 and Bcl-2), GSIS and insulin mRNA levels were measured. F rats developed impairedglucose tolerance (IGT) and a significant increase in plasma triacylglycerols, thiobarbituricacid-reactive substances, insulin levels, homoeostasis model assessment (HOMA)for insulin resistance (HOMA-IR) and B-cell function (HOMA-B) indices. A significant reductionin B-cell mass was associated with an increased apoptotic rate and morphological/ultrastructuralchanges indicative of autophagic activity. All these changes were preventedby either sitagliptin or exendin-4. In cultured islets, F significantly enhanced insulinmRNA and GSIS, decreased Bcl-2 mRNA levels and increased caspase-3 expression.Chloroquine reduced these changes, suggesting the participation of autophagy in this process.Indeed, F induced the increase of both VMP1 expression and LC3-II, suggesting thatVMP1-related autophagy is activated in injured B-cells. Exendin-4 prevented islet-cell damageand autophagy development. VMP1-related autophagy is a reactive process againstF-induced islet dysfunction, being prevented by exendin-4 treatment. This knowledge couldhelp to use autophagy as a potential target for preventing progression from IGT to type 2diabetes mellitus.
Fil: Maiztegui, Barbara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina
Fil: Boggio, Veronica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Román, Carolina Lisi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina
Fil: Flores, Luis Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina
Fil: del Zotto, Hector Herminio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina
Fil: Ropolo, Alejandro Javier. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Grasso, Daniel Hector. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Gagliardino, Juan Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina - Materia
-
B-Cell Function
B-Cell Mass
Autophagy
Incretins - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/63859
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VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretinsMaiztegui, BarbaraBoggio, VeronicaRomán, Carolina LisiFlores, Luis Emiliodel Zotto, Hector HerminioRopolo, Alejandro JavierGrasso, Daniel HectorVaccaro, Maria InesGagliardino, Juan JoseB-Cell FunctionB-Cell MassAutophagyIncretinshttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The aim of the present study was to demonstrate the role of autophagy and incretins inthe fructose-induced alteration of β-cell mass and function. Normal Wistar rats were fed(3 weeks) with a commercial diet without (C) or with 10% fructose in drinking water (F) aloneor plus sitagliptin (CS and FS) or exendin-4 (CE and FE). Serum levels of metabolic/endocrineparameters, B-cell mass, morphology/ultrastructure and apoptosis, vacuole membrane protein1 (VMP1) expression and glucose-stimulated insulin secretion (GSIS) were studied.Complementary to this, islets isolated from normal rats were cultured (3 days) without (C) orwith F and F + exendin-4 or chloroquine. Expression of autophagy-related proteins [VMP1and microtubule-associated protein light chain 3 (LC3)], apoptotic/antiapoptotic markers(caspase-3 and Bcl-2), GSIS and insulin mRNA levels were measured. F rats developed impairedglucose tolerance (IGT) and a significant increase in plasma triacylglycerols, thiobarbituricacid-reactive substances, insulin levels, homoeostasis model assessment (HOMA)for insulin resistance (HOMA-IR) and B-cell function (HOMA-B) indices. A significant reductionin B-cell mass was associated with an increased apoptotic rate and morphological/ultrastructuralchanges indicative of autophagic activity. All these changes were preventedby either sitagliptin or exendin-4. In cultured islets, F significantly enhanced insulinmRNA and GSIS, decreased Bcl-2 mRNA levels and increased caspase-3 expression.Chloroquine reduced these changes, suggesting the participation of autophagy in this process.Indeed, F induced the increase of both VMP1 expression and LC3-II, suggesting thatVMP1-related autophagy is activated in injured B-cells. Exendin-4 prevented islet-cell damageand autophagy development. VMP1-related autophagy is a reactive process againstF-induced islet dysfunction, being prevented by exendin-4 treatment. This knowledge couldhelp to use autophagy as a potential target for preventing progression from IGT to type 2diabetes mellitus.Fil: Maiztegui, Barbara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; ArgentinaFil: Boggio, Veronica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Román, Carolina Lisi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; ArgentinaFil: Flores, Luis Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; ArgentinaFil: del Zotto, Hector Herminio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; ArgentinaFil: Ropolo, Alejandro Javier. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Grasso, Daniel Hector. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Gagliardino, Juan Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; ArgentinaPortland Press2017-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/63859Maiztegui, Barbara; Boggio, Veronica; Román, Carolina Lisi; Flores, Luis Emilio; del Zotto, Hector Herminio; et al.; VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins; Portland Press; Clinical Science; 131; 2-2017; 673-6870143-5221CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.clinsci.org/content/early/2017/02/10/CS20170010info:eu-repo/semantics/altIdentifier/url/http://dx.doi.org/ 10.1042/CS20170010info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:32:04Zoai:ri.conicet.gov.ar:11336/63859instacron: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:34982025-10-15 15:32:05.131CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
title |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
spellingShingle |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins Maiztegui, Barbara B-Cell Function B-Cell Mass Autophagy Incretins |
title_short |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
title_full |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
title_fullStr |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
title_full_unstemmed |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
title_sort |
VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins |
dc.creator.none.fl_str_mv |
Maiztegui, Barbara Boggio, Veronica Román, Carolina Lisi Flores, Luis Emilio del Zotto, Hector Herminio Ropolo, Alejandro Javier Grasso, Daniel Hector Vaccaro, Maria Ines Gagliardino, Juan Jose |
author |
Maiztegui, Barbara |
author_facet |
Maiztegui, Barbara Boggio, Veronica Román, Carolina Lisi Flores, Luis Emilio del Zotto, Hector Herminio Ropolo, Alejandro Javier Grasso, Daniel Hector Vaccaro, Maria Ines Gagliardino, Juan Jose |
author_role |
author |
author2 |
Boggio, Veronica Román, Carolina Lisi Flores, Luis Emilio del Zotto, Hector Herminio Ropolo, Alejandro Javier Grasso, Daniel Hector Vaccaro, Maria Ines Gagliardino, Juan Jose |
author2_role |
author author author author author author author author |
dc.subject.none.fl_str_mv |
B-Cell Function B-Cell Mass Autophagy Incretins |
topic |
B-Cell Function B-Cell Mass Autophagy Incretins |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
The aim of the present study was to demonstrate the role of autophagy and incretins inthe fructose-induced alteration of β-cell mass and function. Normal Wistar rats were fed(3 weeks) with a commercial diet without (C) or with 10% fructose in drinking water (F) aloneor plus sitagliptin (CS and FS) or exendin-4 (CE and FE). Serum levels of metabolic/endocrineparameters, B-cell mass, morphology/ultrastructure and apoptosis, vacuole membrane protein1 (VMP1) expression and glucose-stimulated insulin secretion (GSIS) were studied.Complementary to this, islets isolated from normal rats were cultured (3 days) without (C) orwith F and F + exendin-4 or chloroquine. Expression of autophagy-related proteins [VMP1and microtubule-associated protein light chain 3 (LC3)], apoptotic/antiapoptotic markers(caspase-3 and Bcl-2), GSIS and insulin mRNA levels were measured. F rats developed impairedglucose tolerance (IGT) and a significant increase in plasma triacylglycerols, thiobarbituricacid-reactive substances, insulin levels, homoeostasis model assessment (HOMA)for insulin resistance (HOMA-IR) and B-cell function (HOMA-B) indices. A significant reductionin B-cell mass was associated with an increased apoptotic rate and morphological/ultrastructuralchanges indicative of autophagic activity. All these changes were preventedby either sitagliptin or exendin-4. In cultured islets, F significantly enhanced insulinmRNA and GSIS, decreased Bcl-2 mRNA levels and increased caspase-3 expression.Chloroquine reduced these changes, suggesting the participation of autophagy in this process.Indeed, F induced the increase of both VMP1 expression and LC3-II, suggesting thatVMP1-related autophagy is activated in injured B-cells. Exendin-4 prevented islet-cell damageand autophagy development. VMP1-related autophagy is a reactive process againstF-induced islet dysfunction, being prevented by exendin-4 treatment. This knowledge couldhelp to use autophagy as a potential target for preventing progression from IGT to type 2diabetes mellitus. Fil: Maiztegui, Barbara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina Fil: Boggio, Veronica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina Fil: Román, Carolina Lisi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina Fil: Flores, Luis Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina Fil: del Zotto, Hector Herminio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina Fil: Ropolo, Alejandro Javier. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina Fil: Grasso, Daniel Hector. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina Fil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina Fil: Gagliardino, Juan Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - la Plata. Centro de Endocrinología Experimental y Aplicada. Universidad Nacional de la Plata. Facultad de Ciencias Médicas. Centro de Endocrinología Experimental y Aplicada; Argentina |
description |
The aim of the present study was to demonstrate the role of autophagy and incretins inthe fructose-induced alteration of β-cell mass and function. Normal Wistar rats were fed(3 weeks) with a commercial diet without (C) or with 10% fructose in drinking water (F) aloneor plus sitagliptin (CS and FS) or exendin-4 (CE and FE). Serum levels of metabolic/endocrineparameters, B-cell mass, morphology/ultrastructure and apoptosis, vacuole membrane protein1 (VMP1) expression and glucose-stimulated insulin secretion (GSIS) were studied.Complementary to this, islets isolated from normal rats were cultured (3 days) without (C) orwith F and F + exendin-4 or chloroquine. Expression of autophagy-related proteins [VMP1and microtubule-associated protein light chain 3 (LC3)], apoptotic/antiapoptotic markers(caspase-3 and Bcl-2), GSIS and insulin mRNA levels were measured. F rats developed impairedglucose tolerance (IGT) and a significant increase in plasma triacylglycerols, thiobarbituricacid-reactive substances, insulin levels, homoeostasis model assessment (HOMA)for insulin resistance (HOMA-IR) and B-cell function (HOMA-B) indices. A significant reductionin B-cell mass was associated with an increased apoptotic rate and morphological/ultrastructuralchanges indicative of autophagic activity. All these changes were preventedby either sitagliptin or exendin-4. In cultured islets, F significantly enhanced insulinmRNA and GSIS, decreased Bcl-2 mRNA levels and increased caspase-3 expression.Chloroquine reduced these changes, suggesting the participation of autophagy in this process.Indeed, F induced the increase of both VMP1 expression and LC3-II, suggesting thatVMP1-related autophagy is activated in injured B-cells. Exendin-4 prevented islet-cell damageand autophagy development. VMP1-related autophagy is a reactive process againstF-induced islet dysfunction, being prevented by exendin-4 treatment. This knowledge couldhelp to use autophagy as a potential target for preventing progression from IGT to type 2diabetes mellitus. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-02 |
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/11336/63859 Maiztegui, Barbara; Boggio, Veronica; Román, Carolina Lisi; Flores, Luis Emilio; del Zotto, Hector Herminio; et al.; VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins; Portland Press; Clinical Science; 131; 2-2017; 673-687 0143-5221 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/63859 |
identifier_str_mv |
Maiztegui, Barbara; Boggio, Veronica; Román, Carolina Lisi; Flores, Luis Emilio; del Zotto, Hector Herminio; et al.; VMP1-related autophagy induced by a fructose-rich diet in B-cells: its prevention by incretins; Portland Press; Clinical Science; 131; 2-2017; 673-687 0143-5221 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://www.clinsci.org/content/early/2017/02/10/CS20170010 info:eu-repo/semantics/altIdentifier/url/http://dx.doi.org/ 10.1042/CS20170010 |
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 application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Portland Press |
publisher.none.fl_str_mv |
Portland Press |
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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1846083454956994560 |
score |
13.22299 |