Diabetes impairs heart mitochondrial function without changes in resting cardiac performance

Autores
Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; D'Anunzio, Verónica; Gelpi, Ricardo Jorge; Boveris, Alberto Antonio; Valdez, Laura Batriz
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Diabetes is a chronic disease associated to a cardiac contractile dysfunction that is not attributable to underlying coronaryartery disease or hypertension, and could be consequence of a progressive deterioration of mitochondrial function. Wehypothesized that impaired mitochondrial function precedes Diabetic Cardiomyopathy. Thus, the aim of this work was tostudy the cardiac performance and heart mitochondrial function of diabetic rats, using an experimental model of type I Diabetes.Rats were sacrificed after 28 days of Streptozotocin injection (STZ, 60 mg kg−1, ip.). Heart O2 consumption wasdeclined, mainly due to the impairment of mitochondrial O2 uptake. The mitochondrial dysfunction observed in diabeticanimals included the reduction of state 3 respiration (22%), the decline of ADP/O ratio (∼15%) and the decrease of therespiratory complexes activities (22?26%). An enhancement in mitochondrial H2O2 (127%) and NO (23%) productionrates and in tyrosine nitration (58%) were observed in heart of diabetic rats, with a decrease in Mn-SOD activity (∼50%).Moreover, a decrease in contractile response (38%), inotropic (37%) and lusitropic (58%) reserves were observed in diabeticrats only after a β‐adrenergic stimulus. Therefore, in conditions of sustained hyperglycemia, heart mitochondrialO2 consumption and oxidative phosphorylation efficiency are decreased, and H2O2 and NO productions are increased,leading to a cardiac compromise against a work overload. This mitochondrial impairment was detected in the absence ofheart hypertrophy and of resting cardiac performance changes, suggesting that mitochondrial dysfunction could precedethe onset of diabetic cardiac failure, being H2O2, NO and ATP the molecules probably involved in mitochondrion-cytosolsignalling.
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. 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: D'Anunzio, Verónica. 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: Gelpi, Ricardo Jorge. 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: Boveris, Alberto Antonio. 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: 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
Type I Diabetes
Streptozotocin
Cardiac And Mitochondrial Dysfunction
Mitochondrial Nitric Oxide Synthase
Oxidative Stress
Isoproterenol
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:11336/47596
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47596
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Diabetes impairs heart mitochondrial function without changes in resting cardiac performanceBombicino, Silvina SoniaIglesias, Dario EzequielRukavina Mikusic, Ivana AgustinaD'Anunzio, VerónicaGelpi, Ricardo JorgeBoveris, Alberto AntonioValdez, Laura BatrizType I DiabetesStreptozotocinCardiac And Mitochondrial DysfunctionMitochondrial Nitric Oxide SynthaseOxidative StressIsoproterenolhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Diabetes is a chronic disease associated to a cardiac contractile dysfunction that is not attributable to underlying coronaryartery disease or hypertension, and could be consequence of a progressive deterioration of mitochondrial function. Wehypothesized that impaired mitochondrial function precedes Diabetic Cardiomyopathy. Thus, the aim of this work was tostudy the cardiac performance and heart mitochondrial function of diabetic rats, using an experimental model of type I Diabetes.Rats were sacrificed after 28 days of Streptozotocin injection (STZ, 60 mg kg−1, ip.). Heart O2 consumption wasdeclined, mainly due to the impairment of mitochondrial O2 uptake. The mitochondrial dysfunction observed in diabeticanimals included the reduction of state 3 respiration (22%), the decline of ADP/O ratio (∼15%) and the decrease of therespiratory complexes activities (22?26%). An enhancement in mitochondrial H2O2 (127%) and NO (23%) productionrates and in tyrosine nitration (58%) were observed in heart of diabetic rats, with a decrease in Mn-SOD activity (∼50%).Moreover, a decrease in contractile response (38%), inotropic (37%) and lusitropic (58%) reserves were observed in diabeticrats only after a β‐adrenergic stimulus. Therefore, in conditions of sustained hyperglycemia, heart mitochondrialO2 consumption and oxidative phosphorylation efficiency are decreased, and H2O2 and NO productions are increased,leading to a cardiac compromise against a work overload. This mitochondrial impairment was detected in the absence ofheart hypertrophy and of resting cardiac performance changes, suggesting that mitochondrial dysfunction could precedethe onset of diabetic cardiac failure, being H2O2, NO and ATP the molecules probably involved in mitochondrion-cytosolsignalling.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. 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: D'Anunzio, Verónica. 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: Gelpi, Ricardo Jorge. 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: Boveris, Alberto Antonio. 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: 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; ArgentinaPergamon-Elsevier Science Ltd2016-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47596Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; D'Anunzio, Verónica; Gelpi, Ricardo Jorge; et al.; Diabetes impairs heart mitochondrial function without changes in resting cardiac performance; Pergamon-Elsevier Science Ltd; International Journal of Biochemistry and Cellular Biology; 81; Part B; 12-2016; 335-3451357-2725CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.biocel.2016.09.018info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1357272516302801info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:36:52Zoai:ri.conicet.gov.ar:11336/47596instacron: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 09:36:52.988CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
title Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
spellingShingle Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
Bombicino, Silvina Sonia
Type I Diabetes
Streptozotocin
Cardiac And Mitochondrial Dysfunction
Mitochondrial Nitric Oxide Synthase
Oxidative Stress
Isoproterenol
title_short Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
title_full Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
title_fullStr Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
title_full_unstemmed Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
title_sort Diabetes impairs heart mitochondrial function without changes in resting cardiac performance
dc.creator.none.fl_str_mv Bombicino, Silvina Sonia
Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
D'Anunzio, Verónica
Gelpi, Ricardo Jorge
Boveris, Alberto Antonio
Valdez, Laura Batriz
author Bombicino, Silvina Sonia
author_facet Bombicino, Silvina Sonia
Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
D'Anunzio, Verónica
Gelpi, Ricardo Jorge
Boveris, Alberto Antonio
Valdez, Laura Batriz
author_role author
author2 Iglesias, Dario Ezequiel
Rukavina Mikusic, Ivana Agustina
D'Anunzio, Verónica
Gelpi, Ricardo Jorge
Boveris, Alberto Antonio
Valdez, Laura Batriz
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Type I Diabetes
Streptozotocin
Cardiac And Mitochondrial Dysfunction
Mitochondrial Nitric Oxide Synthase
Oxidative Stress
Isoproterenol
topic Type I Diabetes
Streptozotocin
Cardiac And Mitochondrial Dysfunction
Mitochondrial Nitric Oxide Synthase
Oxidative Stress
Isoproterenol
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Diabetes is a chronic disease associated to a cardiac contractile dysfunction that is not attributable to underlying coronaryartery disease or hypertension, and could be consequence of a progressive deterioration of mitochondrial function. Wehypothesized that impaired mitochondrial function precedes Diabetic Cardiomyopathy. Thus, the aim of this work was tostudy the cardiac performance and heart mitochondrial function of diabetic rats, using an experimental model of type I Diabetes.Rats were sacrificed after 28 days of Streptozotocin injection (STZ, 60 mg kg−1, ip.). Heart O2 consumption wasdeclined, mainly due to the impairment of mitochondrial O2 uptake. The mitochondrial dysfunction observed in diabeticanimals included the reduction of state 3 respiration (22%), the decline of ADP/O ratio (∼15%) and the decrease of therespiratory complexes activities (22?26%). An enhancement in mitochondrial H2O2 (127%) and NO (23%) productionrates and in tyrosine nitration (58%) were observed in heart of diabetic rats, with a decrease in Mn-SOD activity (∼50%).Moreover, a decrease in contractile response (38%), inotropic (37%) and lusitropic (58%) reserves were observed in diabeticrats only after a β‐adrenergic stimulus. Therefore, in conditions of sustained hyperglycemia, heart mitochondrialO2 consumption and oxidative phosphorylation efficiency are decreased, and H2O2 and NO productions are increased,leading to a cardiac compromise against a work overload. This mitochondrial impairment was detected in the absence ofheart hypertrophy and of resting cardiac performance changes, suggesting that mitochondrial dysfunction could precedethe onset of diabetic cardiac failure, being H2O2, NO and ATP the molecules probably involved in mitochondrion-cytosolsignalling.
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. 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: D'Anunzio, Verónica. 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: Gelpi, Ricardo Jorge. 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: Boveris, Alberto Antonio. 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: 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 Diabetes is a chronic disease associated to a cardiac contractile dysfunction that is not attributable to underlying coronaryartery disease or hypertension, and could be consequence of a progressive deterioration of mitochondrial function. Wehypothesized that impaired mitochondrial function precedes Diabetic Cardiomyopathy. Thus, the aim of this work was tostudy the cardiac performance and heart mitochondrial function of diabetic rats, using an experimental model of type I Diabetes.Rats were sacrificed after 28 days of Streptozotocin injection (STZ, 60 mg kg−1, ip.). Heart O2 consumption wasdeclined, mainly due to the impairment of mitochondrial O2 uptake. The mitochondrial dysfunction observed in diabeticanimals included the reduction of state 3 respiration (22%), the decline of ADP/O ratio (∼15%) and the decrease of therespiratory complexes activities (22?26%). An enhancement in mitochondrial H2O2 (127%) and NO (23%) productionrates and in tyrosine nitration (58%) were observed in heart of diabetic rats, with a decrease in Mn-SOD activity (∼50%).Moreover, a decrease in contractile response (38%), inotropic (37%) and lusitropic (58%) reserves were observed in diabeticrats only after a β‐adrenergic stimulus. Therefore, in conditions of sustained hyperglycemia, heart mitochondrialO2 consumption and oxidative phosphorylation efficiency are decreased, and H2O2 and NO productions are increased,leading to a cardiac compromise against a work overload. This mitochondrial impairment was detected in the absence ofheart hypertrophy and of resting cardiac performance changes, suggesting that mitochondrial dysfunction could precedethe onset of diabetic cardiac failure, being H2O2, NO and ATP the molecules probably involved in mitochondrion-cytosolsignalling.
publishDate 2016
dc.date.none.fl_str_mv 2016-12
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/11336/47596
Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; D'Anunzio, Verónica; Gelpi, Ricardo Jorge; et al.; Diabetes impairs heart mitochondrial function without changes in resting cardiac performance; Pergamon-Elsevier Science Ltd; International Journal of Biochemistry and Cellular Biology; 81; Part B; 12-2016; 335-345
1357-2725
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47596
identifier_str_mv Bombicino, Silvina Sonia; Iglesias, Dario Ezequiel; Rukavina Mikusic, Ivana Agustina; D'Anunzio, Verónica; Gelpi, Ricardo Jorge; et al.; Diabetes impairs heart mitochondrial function without changes in resting cardiac performance; Pergamon-Elsevier Science Ltd; International Journal of Biochemistry and Cellular Biology; 81; Part B; 12-2016; 335-345
1357-2725
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.biocel.2016.09.018
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1357272516302801
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
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
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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