Heart mitochondrial dysfunction in diabetic rats

Autores
Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; Boveris, Alberto Antonio; Valdez, Laura Batriz
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. In streptozotocin-induced diabetic rats, alterations in contractile response and lusitropic reserve, after β adrenergic stimuli, were observed. Additionally, tissue O2 consumption was declined. A condition of mitochondrial dysfunction with decreased mitochondrial state 3 O2 consumption, respiratory control ratio, mitochondrial respiratory complexes activities and ATP production were present in hearts of diabetic animals. We observed an increase in mitochondrial NO production and in cytochrome oxidase activity measured in heart homogenates. This latter suggests an increase of new mitochondria. Thus, the impairment of mitochondrial function with enhancement in mitochondrial biogenesis could precede the onset of diabetic cardiomyopathy. However, mitochondrial biogenesis does not necessarily imply that resultant mitochondria are functional; this might explain the impairment in cardiac energy metabolism that occurs in hearts of diabetic rats.
Fil: Bombicino, Silvina Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Iglesias, Dario Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Rukavina Mikusic, Ivana Agustina. No especifica;
Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Materia
DIABETES
DIABETIC CARDIOMYOPATHY
HEART
MITOCHONDRIA
NITRIC OXIDE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/49590
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/49590
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Heart mitochondrial dysfunction in diabetic ratsBombicino, Silvina SoniaIglesias, Dario EzequielRukavina Mikusic, Ivana AgustinaBoveris, Alberto AntonioValdez, Laura BatrizDIABETESDIABETIC CARDIOMYOPATHYHEARTMITOCHONDRIANITRIC OXIDEhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. In streptozotocin-induced diabetic rats, alterations in contractile response and lusitropic reserve, after β adrenergic stimuli, were observed. Additionally, tissue O2 consumption was declined. A condition of mitochondrial dysfunction with decreased mitochondrial state 3 O2 consumption, respiratory control ratio, mitochondrial respiratory complexes activities and ATP production were present in hearts of diabetic animals. We observed an increase in mitochondrial NO production and in cytochrome oxidase activity measured in heart homogenates. This latter suggests an increase of new mitochondria. Thus, the impairment of mitochondrial function with enhancement in mitochondrial biogenesis could precede the onset of diabetic cardiomyopathy. However, mitochondrial biogenesis does not necessarily imply that resultant mitochondria are functional; this might explain the impairment in cardiac energy metabolism that occurs in hearts of diabetic rats.Fil: Bombicino, Silvina Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Iglesias, Dario Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Rukavina Mikusic, Ivana Agustina. No especifica;Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaSociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas2016-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/49590Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; Boveris, Alberto Antonio; Valdez, Laura Batriz; Heart mitochondrial dysfunction in diabetic rats; Sociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas; Biocell; 40; 1; 4-2016; 7-101667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mendoza-conicet.gob.ar/portal/biocell/vol/pdf/40_1/Biocell_MS5002_Bombicino.pdfinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:29:58Zoai:ri.conicet.gov.ar:11336/49590instacron: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 10:29:58.305CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Heart mitochondrial dysfunction in diabetic rats
title Heart mitochondrial dysfunction in diabetic rats
spellingShingle Heart mitochondrial dysfunction in diabetic rats
Bombicino, Silvina Sonia
DIABETES
DIABETIC CARDIOMYOPATHY
HEART
MITOCHONDRIA
NITRIC OXIDE
title_short Heart mitochondrial dysfunction in diabetic rats
title_full Heart mitochondrial dysfunction in diabetic rats
title_fullStr Heart mitochondrial dysfunction in diabetic rats
title_full_unstemmed Heart mitochondrial dysfunction in diabetic rats
title_sort Heart mitochondrial dysfunction in diabetic rats
dc.creator.none.fl_str_mv Bombicino, Silvina Sonia
Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
Boveris, Alberto Antonio
Valdez, Laura Batriz
author Bombicino, Silvina Sonia
author_facet Bombicino, Silvina Sonia
Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
Boveris, Alberto Antonio
Valdez, Laura Batriz
author_role author
author2 Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
Boveris, Alberto Antonio
Valdez, Laura Batriz
author2_role author
author
author
author
dc.subject.none.fl_str_mv DIABETES
DIABETIC CARDIOMYOPATHY
HEART
MITOCHONDRIA
NITRIC OXIDE
topic DIABETES
DIABETIC CARDIOMYOPATHY
HEART
MITOCHONDRIA
NITRIC OXIDE
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. In streptozotocin-induced diabetic rats, alterations in contractile response and lusitropic reserve, after β adrenergic stimuli, were observed. Additionally, tissue O2 consumption was declined. A condition of mitochondrial dysfunction with decreased mitochondrial state 3 O2 consumption, respiratory control ratio, mitochondrial respiratory complexes activities and ATP production were present in hearts of diabetic animals. We observed an increase in mitochondrial NO production and in cytochrome oxidase activity measured in heart homogenates. This latter suggests an increase of new mitochondria. Thus, the impairment of mitochondrial function with enhancement in mitochondrial biogenesis could precede the onset of diabetic cardiomyopathy. However, mitochondrial biogenesis does not necessarily imply that resultant mitochondria are functional; this might explain the impairment in cardiac energy metabolism that occurs in hearts of diabetic rats.
Fil: Bombicino, Silvina Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Iglesias, Dario Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Rukavina Mikusic, Ivana Agustina. No especifica;
Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
description Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. In streptozotocin-induced diabetic rats, alterations in contractile response and lusitropic reserve, after β adrenergic stimuli, were observed. Additionally, tissue O2 consumption was declined. A condition of mitochondrial dysfunction with decreased mitochondrial state 3 O2 consumption, respiratory control ratio, mitochondrial respiratory complexes activities and ATP production were present in hearts of diabetic animals. We observed an increase in mitochondrial NO production and in cytochrome oxidase activity measured in heart homogenates. This latter suggests an increase of new mitochondria. Thus, the impairment of mitochondrial function with enhancement in mitochondrial biogenesis could precede the onset of diabetic cardiomyopathy. However, mitochondrial biogenesis does not necessarily imply that resultant mitochondria are functional; this might explain the impairment in cardiac energy metabolism that occurs in hearts of diabetic rats.
publishDate 2016
dc.date.none.fl_str_mv 2016-04
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/11336/49590
Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; Boveris, Alberto Antonio; Valdez, Laura Batriz; Heart mitochondrial dysfunction in diabetic rats; Sociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas; Biocell; 40; 1; 4-2016; 7-10
1667-5746
CONICET Digital
CONICET
url http://hdl.handle.net/11336/49590
identifier_str_mv Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; Boveris, Alberto Antonio; Valdez, Laura Batriz; Heart mitochondrial dysfunction in diabetic rats; Sociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas; Biocell; 40; 1; 4-2016; 7-10
1667-5746
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://www.mendoza-conicet.gob.ar/portal/biocell/vol/pdf/40_1/Biocell_MS5002_Bombicino.pdf
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Sociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas
publisher.none.fl_str_mv Sociedad Latinoamericana de Microscopía Electrónica; Centro Regional de Investigaciones Científicas y Tecnológicas
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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score 13.070432

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