Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance

Autores
Molina, Marisa Nile; Ferder, León; Manucha, Walter Ariel Fernando
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Insulin resistance (IR) is present in pathologies such as diabetes, obesity, metabolic syndrome, impaired glucose tolerance, hypertension, inflammation, cardiac disease, and dyslipidemias. Population studies show that IR is multifactorial and has genetic components, such as defects in the insulin-signaling pathway (as serine phosphorylation on insulin substrate or decreased activation of signaling molecules) and RAS/MAPK-dependent pathways. IR is connected to mitochondrial dysfunction, overproduction of oxidants, accumulation of fat, and an over-activation of the renin-angiotensin system linked to the NADPH oxidase activity. In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. However, increased NO may promote vasculoprotection. Moreover, reduced NO release induces heat shock protein 70 kDa (HSP70) expression in IR and diabetes, mediating beneficial effects against oxidative stress injury, inflammation and apoptosis. HSP70 may be used as biomarker of the chronicity of diabetes. Hsp72 (inducible protein) is linked to vascular complications with a high-fat diet by blocking inflammation signaling (cytoprotective and anti-cytotoxicity intracellular role). Elucidating the IR signaling pathways and the roles of NO and HSPs is relevant to the application of new treatments, such as heat shock and thermal therapy, nitrosylated drugs, chemical chaperones or exercise training.
Fil: Molina, Marisa Nile. Universidad "Juan Agustín Maza". Facultad de Farmacia y Bioquímica; Argentina
Fil: Ferder, León. Universidad de Puerto Rico; Puerto Rico
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Materia
Heat Shock Protein 70
Insulin Resistance
Nitric Oxide
Oxidative Stress
Type-2 Diabetes Mellitus
Vitamin D
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:11336/79151
Acceder
id CONICETDig_4f3be66f956f79da4d6b52a8d3115118
oai_identifier_str oai:ri.conicet.gov.ar:11336/79151
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin ResistanceMolina, Marisa NileFerder, LeónManucha, Walter Ariel FernandoHeat Shock Protein 70Insulin ResistanceNitric OxideOxidative StressType-2 Diabetes MellitusVitamin Dhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Insulin resistance (IR) is present in pathologies such as diabetes, obesity, metabolic syndrome, impaired glucose tolerance, hypertension, inflammation, cardiac disease, and dyslipidemias. Population studies show that IR is multifactorial and has genetic components, such as defects in the insulin-signaling pathway (as serine phosphorylation on insulin substrate or decreased activation of signaling molecules) and RAS/MAPK-dependent pathways. IR is connected to mitochondrial dysfunction, overproduction of oxidants, accumulation of fat, and an over-activation of the renin-angiotensin system linked to the NADPH oxidase activity. In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. However, increased NO may promote vasculoprotection. Moreover, reduced NO release induces heat shock protein 70 kDa (HSP70) expression in IR and diabetes, mediating beneficial effects against oxidative stress injury, inflammation and apoptosis. HSP70 may be used as biomarker of the chronicity of diabetes. Hsp72 (inducible protein) is linked to vascular complications with a high-fat diet by blocking inflammation signaling (cytoprotective and anti-cytotoxicity intracellular role). Elucidating the IR signaling pathways and the roles of NO and HSPs is relevant to the application of new treatments, such as heat shock and thermal therapy, nitrosylated drugs, chemical chaperones or exercise training.Fil: Molina, Marisa Nile. Universidad "Juan Agustín Maza". Facultad de Farmacia y Bioquímica; ArgentinaFil: Ferder, León. Universidad de Puerto Rico; Puerto RicoFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaSpringer2016-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/79151Molina, Marisa Nile; Ferder, León; Manucha, Walter Ariel Fernando; Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance; Springer; Current Hypertension Reports; 18; 1; 1-2016; 1-131522-6417CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://link.springer.com/article/10.1007/s11906-015-0615-4info:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-015-0615-4info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:09:47Zoai:ri.conicet.gov.ar:11336/79151instacron: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 11:09:48.244CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
title Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
spellingShingle Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
Molina, Marisa Nile
Heat Shock Protein 70
Insulin Resistance
Nitric Oxide
Oxidative Stress
Type-2 Diabetes Mellitus
Vitamin D
title_short Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
title_full Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
title_fullStr Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
title_full_unstemmed Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
title_sort Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance
dc.creator.none.fl_str_mv Molina, Marisa Nile
Ferder, León
Manucha, Walter Ariel Fernando
author Molina, Marisa Nile
author_facet Molina, Marisa Nile
Ferder, León
Manucha, Walter Ariel Fernando
author_role author
author2 Ferder, León
Manucha, Walter Ariel Fernando
author2_role author
author
dc.subject.none.fl_str_mv Heat Shock Protein 70
Insulin Resistance
Nitric Oxide
Oxidative Stress
Type-2 Diabetes Mellitus
Vitamin D
topic Heat Shock Protein 70
Insulin Resistance
Nitric Oxide
Oxidative Stress
Type-2 Diabetes Mellitus
Vitamin D
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Insulin resistance (IR) is present in pathologies such as diabetes, obesity, metabolic syndrome, impaired glucose tolerance, hypertension, inflammation, cardiac disease, and dyslipidemias. Population studies show that IR is multifactorial and has genetic components, such as defects in the insulin-signaling pathway (as serine phosphorylation on insulin substrate or decreased activation of signaling molecules) and RAS/MAPK-dependent pathways. IR is connected to mitochondrial dysfunction, overproduction of oxidants, accumulation of fat, and an over-activation of the renin-angiotensin system linked to the NADPH oxidase activity. In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. However, increased NO may promote vasculoprotection. Moreover, reduced NO release induces heat shock protein 70 kDa (HSP70) expression in IR and diabetes, mediating beneficial effects against oxidative stress injury, inflammation and apoptosis. HSP70 may be used as biomarker of the chronicity of diabetes. Hsp72 (inducible protein) is linked to vascular complications with a high-fat diet by blocking inflammation signaling (cytoprotective and anti-cytotoxicity intracellular role). Elucidating the IR signaling pathways and the roles of NO and HSPs is relevant to the application of new treatments, such as heat shock and thermal therapy, nitrosylated drugs, chemical chaperones or exercise training.
Fil: Molina, Marisa Nile. Universidad "Juan Agustín Maza". Facultad de Farmacia y Bioquímica; Argentina
Fil: Ferder, León. Universidad de Puerto Rico; Puerto Rico
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
description Insulin resistance (IR) is present in pathologies such as diabetes, obesity, metabolic syndrome, impaired glucose tolerance, hypertension, inflammation, cardiac disease, and dyslipidemias. Population studies show that IR is multifactorial and has genetic components, such as defects in the insulin-signaling pathway (as serine phosphorylation on insulin substrate or decreased activation of signaling molecules) and RAS/MAPK-dependent pathways. IR is connected to mitochondrial dysfunction, overproduction of oxidants, accumulation of fat, and an over-activation of the renin-angiotensin system linked to the NADPH oxidase activity. In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. However, increased NO may promote vasculoprotection. Moreover, reduced NO release induces heat shock protein 70 kDa (HSP70) expression in IR and diabetes, mediating beneficial effects against oxidative stress injury, inflammation and apoptosis. HSP70 may be used as biomarker of the chronicity of diabetes. Hsp72 (inducible protein) is linked to vascular complications with a high-fat diet by blocking inflammation signaling (cytoprotective and anti-cytotoxicity intracellular role). Elucidating the IR signaling pathways and the roles of NO and HSPs is relevant to the application of new treatments, such as heat shock and thermal therapy, nitrosylated drugs, chemical chaperones or exercise training.
publishDate 2016
dc.date.none.fl_str_mv 2016-01
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/11336/79151
Molina, Marisa Nile; Ferder, León; Manucha, Walter Ariel Fernando; Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance; Springer; Current Hypertension Reports; 18; 1; 1-2016; 1-13
1522-6417
CONICET Digital
CONICET
url http://hdl.handle.net/11336/79151
identifier_str_mv Molina, Marisa Nile; Ferder, León; Manucha, Walter Ariel Fernando; Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance; Springer; Current Hypertension Reports; 18; 1; 1-2016; 1-13
1522-6417
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://link.springer.com/article/10.1007/s11906-015-0615-4
info:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-015-0615-4
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
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
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
_version_ 1846781450060300288
score 13.144186

Publicaciones similares