Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Arquivos Brasileiros de Cardiologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2019001201139 |
Resumo: | Abstract Obesity associated with systemic inflammation induces insulin resistance (IR), with consequent chronic hyperglycemia. A series of reactions are involved in this process, including increased release of proinflammatory cytokines, and activation of c-Jun N-terminal kinase (JNK), nuclear factor-kappa B (NF-κB) and toll-like receptor 4 (TLR4) receptors. Among the therapeutic tools available nowadays, physical exercise (PE) has a known hypoglycemic effect explained by complex molecular mechanisms, including an increase in insulin receptor phosphorylation, in AMP-activated protein kinase (AMPK) activity, in the Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) pathway, with subsequent activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), Rac1, TBC1 domain family member 1 and 4 (TBC1D1 and TBC1D4), in addition to a variety of signaling molecules, such as GTPases, Rab and soluble N-ethylmaleimide-sensitive factor attached protein receptor (SNARE) proteins. These pathways promote greater translocation of GLUT4 and consequent glucose uptake by the skeletal muscle. Phosphoinositide-dependent kinase (PDK), atypical protein kinase C (aPKC) and some of its isoforms, such as PKC-iota/lambda also seem to play a fundamental role in the transport of glucose. In this sense, the association between autophagy and exercise has also demonstrated a relevant role in the uptake of muscle glucose. Insulin, in turn, uses a phosphoinositide 3-kinase (PI3K)-dependent mechanism, while exercise signal may be triggered by the release of calcium from the sarcoplasmic reticulum. The objective of this review is to describe the main molecular mechanisms of IR and the relationship between PE and glucose uptake. |
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Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of InflammationExerciseInsulin ResistanceChronic InflammationGlucose Metabolism DisordersAnti-Inflammatoty AgentsGlucose Transporter Type 4Abstract Obesity associated with systemic inflammation induces insulin resistance (IR), with consequent chronic hyperglycemia. A series of reactions are involved in this process, including increased release of proinflammatory cytokines, and activation of c-Jun N-terminal kinase (JNK), nuclear factor-kappa B (NF-κB) and toll-like receptor 4 (TLR4) receptors. Among the therapeutic tools available nowadays, physical exercise (PE) has a known hypoglycemic effect explained by complex molecular mechanisms, including an increase in insulin receptor phosphorylation, in AMP-activated protein kinase (AMPK) activity, in the Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) pathway, with subsequent activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), Rac1, TBC1 domain family member 1 and 4 (TBC1D1 and TBC1D4), in addition to a variety of signaling molecules, such as GTPases, Rab and soluble N-ethylmaleimide-sensitive factor attached protein receptor (SNARE) proteins. These pathways promote greater translocation of GLUT4 and consequent glucose uptake by the skeletal muscle. Phosphoinositide-dependent kinase (PDK), atypical protein kinase C (aPKC) and some of its isoforms, such as PKC-iota/lambda also seem to play a fundamental role in the transport of glucose. In this sense, the association between autophagy and exercise has also demonstrated a relevant role in the uptake of muscle glucose. Insulin, in turn, uses a phosphoinositide 3-kinase (PI3K)-dependent mechanism, while exercise signal may be triggered by the release of calcium from the sarcoplasmic reticulum. The objective of this review is to describe the main molecular mechanisms of IR and the relationship between PE and glucose uptake.Sociedade Brasileira de Cardiologia - SBC2019-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2019001201139Arquivos Brasileiros de Cardiologia v.113 n.6 2019reponame:Arquivos Brasileiros de Cardiologia (Online)instname:Sociedade Brasileira de Cardiologia (SBC)instacron:SBC10.5935/abc.20190224info:eu-repo/semantics/openAccessFerrari,FilipeBock,Patrícia MartinsMotta,Marcelo TrotteHelal,Lucaseng2020-03-16T00:00:00Zoai:scielo:S0066-782X2019001201139Revistahttp://www.arquivosonline.com.br/https://old.scielo.br/oai/scielo-oai.php||arquivos@cardiol.br1678-41700066-782Xopendoar:2020-03-16T00:00Arquivos Brasileiros de Cardiologia (Online) - Sociedade Brasileira de Cardiologia (SBC)false |
dc.title.none.fl_str_mv |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
title |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
spellingShingle |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation Ferrari,Filipe Exercise Insulin Resistance Chronic Inflammation Glucose Metabolism Disorders Anti-Inflammatoty Agents Glucose Transporter Type 4 |
title_short |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
title_full |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
title_fullStr |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
title_full_unstemmed |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
title_sort |
Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation |
author |
Ferrari,Filipe |
author_facet |
Ferrari,Filipe Bock,Patrícia Martins Motta,Marcelo Trotte Helal,Lucas |
author_role |
author |
author2 |
Bock,Patrícia Martins Motta,Marcelo Trotte Helal,Lucas |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Ferrari,Filipe Bock,Patrícia Martins Motta,Marcelo Trotte Helal,Lucas |
dc.subject.por.fl_str_mv |
Exercise Insulin Resistance Chronic Inflammation Glucose Metabolism Disorders Anti-Inflammatoty Agents Glucose Transporter Type 4 |
topic |
Exercise Insulin Resistance Chronic Inflammation Glucose Metabolism Disorders Anti-Inflammatoty Agents Glucose Transporter Type 4 |
description |
Abstract Obesity associated with systemic inflammation induces insulin resistance (IR), with consequent chronic hyperglycemia. A series of reactions are involved in this process, including increased release of proinflammatory cytokines, and activation of c-Jun N-terminal kinase (JNK), nuclear factor-kappa B (NF-κB) and toll-like receptor 4 (TLR4) receptors. Among the therapeutic tools available nowadays, physical exercise (PE) has a known hypoglycemic effect explained by complex molecular mechanisms, including an increase in insulin receptor phosphorylation, in AMP-activated protein kinase (AMPK) activity, in the Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) pathway, with subsequent activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), Rac1, TBC1 domain family member 1 and 4 (TBC1D1 and TBC1D4), in addition to a variety of signaling molecules, such as GTPases, Rab and soluble N-ethylmaleimide-sensitive factor attached protein receptor (SNARE) proteins. These pathways promote greater translocation of GLUT4 and consequent glucose uptake by the skeletal muscle. Phosphoinositide-dependent kinase (PDK), atypical protein kinase C (aPKC) and some of its isoforms, such as PKC-iota/lambda also seem to play a fundamental role in the transport of glucose. In this sense, the association between autophagy and exercise has also demonstrated a relevant role in the uptake of muscle glucose. Insulin, in turn, uses a phosphoinositide 3-kinase (PI3K)-dependent mechanism, while exercise signal may be triggered by the release of calcium from the sarcoplasmic reticulum. The objective of this review is to describe the main molecular mechanisms of IR and the relationship between PE and glucose uptake. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-12-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2019001201139 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2019001201139 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.5935/abc.20190224 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Cardiologia - SBC |
publisher.none.fl_str_mv |
Sociedade Brasileira de Cardiologia - SBC |
dc.source.none.fl_str_mv |
Arquivos Brasileiros de Cardiologia v.113 n.6 2019 reponame:Arquivos Brasileiros de Cardiologia (Online) instname:Sociedade Brasileira de Cardiologia (SBC) instacron:SBC |
instname_str |
Sociedade Brasileira de Cardiologia (SBC) |
instacron_str |
SBC |
institution |
SBC |
reponame_str |
Arquivos Brasileiros de Cardiologia (Online) |
collection |
Arquivos Brasileiros de Cardiologia (Online) |
repository.name.fl_str_mv |
Arquivos Brasileiros de Cardiologia (Online) - Sociedade Brasileira de Cardiologia (SBC) |
repository.mail.fl_str_mv |
||arquivos@cardiol.br |
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1752126569737879552 |