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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/49590
Ver los metadatos del registro completo
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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 Técnicas2025-09-03T10:06:24Zoai: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:34982025-09-03 10:06:25.153CONICET 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 |
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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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1842269957701763072 |
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13.13397 |