Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice

Autores
Rubinstein Guichon, Mara Roxana; Wydra, Laura; Bianchi, Maria Silvia; Wald, Miriam Ruth; Genaro, Ana Maria
Año de publicación
2022
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Type 1 diabetes (T1D) is characterized by impaired insulin secretion and it has been recognized the contribution of psychosocial factors (including chronic stress exposure) in T1D. Gut microbiota is the group of microorganisms (commensal, symbiotic and pathogenic) that we find in our gut. It participates in multiple functions and an association between unbalanced microbiota and several diseases, including diabetes, has been reported. NOD/ShiLtJ mice are a model for autoimmune type 1 diabetes. The aim of the present work is to study the effect of chronic stress in diabetes development and to characterize the microbiota alterations in NOD/ShiLtJ mice. For this purpose, the animals were subject to chronic stress (CS) by the application of aleatory and unpredictable stressors. NOD/ShiLtJ mice exposed to CS (NOD + CS) showed an increase in diabetes incidence (Long-rank test, p<0.05) and higher glycemia levels (t test, p<0.001). Serum samples were collected and the titter for autoantibodies against insulin was measured by ELISA. NOD + CS had a lower antibody titer (t test, p<0.05). To determine microbiota alterations, fecal samples were collected and genomic DNA was extracted. 16s total bacteria, 16s Bacteriodetes and 16s Firmicutes (the most abundant components of the microbiota) were measured by qPCR using specific primers. No changes were detected in 16s total bacteria and 16s Firmicutes but a decrease in 16s Bacteroidetes was found in NOD + CS (t test p<0.05). These results show that CS has a role in type 1 diabetes development and alters gut microbiota composition, and they could suggest that the decrease in 16s bacteroidetes may participate in type 1 diabetes development.
Fil: Rubinstein Guichon, Mara Roxana. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Wydra, Laura. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bianchi, Maria Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Wald, Miriam Ruth. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Genaro, Ana Maria. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología
Mar del plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
Materia
Type 1 diabetes
Chronic Stress
Microbiota
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:11336/260672

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network_name_str CONICET Digital (CONICET)
spelling Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj miceRubinstein Guichon, Mara RoxanaWydra, LauraBianchi, Maria SilviaWald, Miriam RuthGenaro, Ana MariaType 1 diabetesChronic StressMicrobiotahttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Type 1 diabetes (T1D) is characterized by impaired insulin secretion and it has been recognized the contribution of psychosocial factors (including chronic stress exposure) in T1D. Gut microbiota is the group of microorganisms (commensal, symbiotic and pathogenic) that we find in our gut. It participates in multiple functions and an association between unbalanced microbiota and several diseases, including diabetes, has been reported. NOD/ShiLtJ mice are a model for autoimmune type 1 diabetes. The aim of the present work is to study the effect of chronic stress in diabetes development and to characterize the microbiota alterations in NOD/ShiLtJ mice. For this purpose, the animals were subject to chronic stress (CS) by the application of aleatory and unpredictable stressors. NOD/ShiLtJ mice exposed to CS (NOD + CS) showed an increase in diabetes incidence (Long-rank test, p<0.05) and higher glycemia levels (t test, p<0.001). Serum samples were collected and the titter for autoantibodies against insulin was measured by ELISA. NOD + CS had a lower antibody titer (t test, p<0.05). To determine microbiota alterations, fecal samples were collected and genomic DNA was extracted. 16s total bacteria, 16s Bacteriodetes and 16s Firmicutes (the most abundant components of the microbiota) were measured by qPCR using specific primers. No changes were detected in 16s total bacteria and 16s Firmicutes but a decrease in 16s Bacteroidetes was found in NOD + CS (t test p<0.05). These results show that CS has a role in type 1 diabetes development and alters gut microbiota composition, and they could suggest that the decrease in 16s bacteroidetes may participate in type 1 diabetes development.Fil: Rubinstein Guichon, Mara Roxana. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Wydra, Laura. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Bianchi, Maria Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Wald, Miriam Ruth. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Genaro, Ana Maria. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaLXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de FisiologíaMar del plataArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaSociedad Argentina de FisiologíaFundación Revista Medicina2022info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentapplication/pdfhttp://hdl.handle.net/11336/260672Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del plata; Argentina; 2022; 1-11669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://medicinabuenosaires.com/revistas/vol82-22/s5/1s5.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:18:39Zoai:ri.conicet.gov.ar:11336/260672instacron: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:34982025-10-22 12:18:39.951CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
title Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
spellingShingle Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
Rubinstein Guichon, Mara Roxana
Type 1 diabetes
Chronic Stress
Microbiota
title_short Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
title_full Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
title_fullStr Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
title_full_unstemmed Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
title_sort Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice
dc.creator.none.fl_str_mv Rubinstein Guichon, Mara Roxana
Wydra, Laura
Bianchi, Maria Silvia
Wald, Miriam Ruth
Genaro, Ana Maria
author Rubinstein Guichon, Mara Roxana
author_facet Rubinstein Guichon, Mara Roxana
Wydra, Laura
Bianchi, Maria Silvia
Wald, Miriam Ruth
Genaro, Ana Maria
author_role author
author2 Wydra, Laura
Bianchi, Maria Silvia
Wald, Miriam Ruth
Genaro, Ana Maria
author2_role author
author
author
author
dc.subject.none.fl_str_mv Type 1 diabetes
Chronic Stress
Microbiota
topic Type 1 diabetes
Chronic Stress
Microbiota
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Type 1 diabetes (T1D) is characterized by impaired insulin secretion and it has been recognized the contribution of psychosocial factors (including chronic stress exposure) in T1D. Gut microbiota is the group of microorganisms (commensal, symbiotic and pathogenic) that we find in our gut. It participates in multiple functions and an association between unbalanced microbiota and several diseases, including diabetes, has been reported. NOD/ShiLtJ mice are a model for autoimmune type 1 diabetes. The aim of the present work is to study the effect of chronic stress in diabetes development and to characterize the microbiota alterations in NOD/ShiLtJ mice. For this purpose, the animals were subject to chronic stress (CS) by the application of aleatory and unpredictable stressors. NOD/ShiLtJ mice exposed to CS (NOD + CS) showed an increase in diabetes incidence (Long-rank test, p<0.05) and higher glycemia levels (t test, p<0.001). Serum samples were collected and the titter for autoantibodies against insulin was measured by ELISA. NOD + CS had a lower antibody titer (t test, p<0.05). To determine microbiota alterations, fecal samples were collected and genomic DNA was extracted. 16s total bacteria, 16s Bacteriodetes and 16s Firmicutes (the most abundant components of the microbiota) were measured by qPCR using specific primers. No changes were detected in 16s total bacteria and 16s Firmicutes but a decrease in 16s Bacteroidetes was found in NOD + CS (t test p<0.05). These results show that CS has a role in type 1 diabetes development and alters gut microbiota composition, and they could suggest that the decrease in 16s bacteroidetes may participate in type 1 diabetes development.
Fil: Rubinstein Guichon, Mara Roxana. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Wydra, Laura. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bianchi, Maria Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Wald, Miriam Ruth. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Genaro, Ana Maria. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología
Mar del plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
description Type 1 diabetes (T1D) is characterized by impaired insulin secretion and it has been recognized the contribution of psychosocial factors (including chronic stress exposure) in T1D. Gut microbiota is the group of microorganisms (commensal, symbiotic and pathogenic) that we find in our gut. It participates in multiple functions and an association between unbalanced microbiota and several diseases, including diabetes, has been reported. NOD/ShiLtJ mice are a model for autoimmune type 1 diabetes. The aim of the present work is to study the effect of chronic stress in diabetes development and to characterize the microbiota alterations in NOD/ShiLtJ mice. For this purpose, the animals were subject to chronic stress (CS) by the application of aleatory and unpredictable stressors. NOD/ShiLtJ mice exposed to CS (NOD + CS) showed an increase in diabetes incidence (Long-rank test, p<0.05) and higher glycemia levels (t test, p<0.001). Serum samples were collected and the titter for autoantibodies against insulin was measured by ELISA. NOD + CS had a lower antibody titer (t test, p<0.05). To determine microbiota alterations, fecal samples were collected and genomic DNA was extracted. 16s total bacteria, 16s Bacteriodetes and 16s Firmicutes (the most abundant components of the microbiota) were measured by qPCR using specific primers. No changes were detected in 16s total bacteria and 16s Firmicutes but a decrease in 16s Bacteroidetes was found in NOD + CS (t test p<0.05). These results show that CS has a role in type 1 diabetes development and alters gut microbiota composition, and they could suggest that the decrease in 16s bacteroidetes may participate in type 1 diabetes development.
publishDate 2022
dc.date.none.fl_str_mv 2022
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dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/260672
Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del plata; Argentina; 2022; 1-1
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/260672
identifier_str_mv Chronic stress exposure increases diabetes incidence and alters gut microbiota in nod/shiltj mice; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del plata; Argentina; 2022; 1-1
1669-9106
CONICET Digital
CONICET
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