Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1

Detalhes bibliográficos
Autor(a) principal: Dib, Sergio Atala [UNIFESP]
Data de Publicação: 2006
Tipo de documento: Artigo
Idioma: por
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1590/S0004-27302006000200011
http://repositorio.unifesp.br/handle/11600/2995
Resumo: Insulin resistance (IR) plays a larger role in the type 1 diabetes mellitus (T1DM) disease process than commonly recognized. Overweight and physical inactivity have increased steadily for the last 20-30 years in children and adolescents in many populations, concurrently with a rising incidence of T1DM. The role of IR in T1DM has only recently been gaining acceptance. This review will focus on how IR influences our current understanding of disease development and metabolic syndrome (MS) in T1DM. Increases in IR by weight gain and sedentarism, associated to decreased beta cell mass by autoimmune process, may disrupt normoglycemia in pre-T1DM individuals. IR may reflect a more aggressive form of autoimmune disease mediated by immuno-inflammatory factors that also mediate beta cell destruction (TNF-alpha and IL-6). These concepts are included in the accelerator hypothesis. Moreover, family history of T2DM and chronic hyperglycemia (glucotoxicity), occurring after T1DM diagnosis, contribute to decrease peripheral glucose uptake. The onset of diabetic nephropathy (DN) might also contribute to IR and metabolic syndrome (MS) via low-grade inflammation and increased oxidative stress. MS is found between 12 to 40% in T1DM, especially in patients with advanced DN and poor glycemic control. These findings have therapeutic and cardiovascular prognostic implications as children make the transition toward adolescence and young adulthood T1DM.
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spelling Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1Insulin resistance and metabolic syndrome in type 1 diabetes mellitusInsulin resistanceMetabolic syndromeType 1 diabetes mellitusResistência à insulinaSíndrome metabólicaDiabetes melito do tipo 1Insulin resistance (IR) plays a larger role in the type 1 diabetes mellitus (T1DM) disease process than commonly recognized. Overweight and physical inactivity have increased steadily for the last 20-30 years in children and adolescents in many populations, concurrently with a rising incidence of T1DM. The role of IR in T1DM has only recently been gaining acceptance. This review will focus on how IR influences our current understanding of disease development and metabolic syndrome (MS) in T1DM. Increases in IR by weight gain and sedentarism, associated to decreased beta cell mass by autoimmune process, may disrupt normoglycemia in pre-T1DM individuals. IR may reflect a more aggressive form of autoimmune disease mediated by immuno-inflammatory factors that also mediate beta cell destruction (TNF-alpha and IL-6). These concepts are included in the accelerator hypothesis. Moreover, family history of T2DM and chronic hyperglycemia (glucotoxicity), occurring after T1DM diagnosis, contribute to decrease peripheral glucose uptake. The onset of diabetic nephropathy (DN) might also contribute to IR and metabolic syndrome (MS) via low-grade inflammation and increased oxidative stress. MS is found between 12 to 40% in T1DM, especially in patients with advanced DN and poor glycemic control. These findings have therapeutic and cardiovascular prognostic implications as children make the transition toward adolescence and young adulthood T1DM.A resistência à insulina (RI) pode desempenhar um papel, na história natural do diabetes melito do tipo 1 (DM1), maior do que o habitualmente reconhecido. Nas últimas décadas, este papel se tornou mais evidente com o aumento da obesidade e da diminuição da atividade física nos jovens. Esta revisão tem como objetivo apresentar e discutir a RI nas diferentes fases do DM1, bem como a prevalência da Síndrome Metabólica (SM) nessa condição. O aumento na RI, concomitante a uma diminuição da massa de células beta, pode alterar o equilíbrio entre a sensibilidade à insulina e a secreção de insulina, e precipitar a hiperglicemia nos indivíduos com pré-DM1. A RI poderia refletir uma forma mais agressiva de doença autoimune, mediada por fatores imuno-inflamatórios, comuns a ambos os processos, que também mediassem a destruição das células beta (TNF-alfa e IL-6). Estes conceitos fazem parte da Hipótese Aceleradora. A história familiar de DM2 e a hiperglicemia crônica (glicotoxicidade), durante a fase clínica do DM1, estão associadas a uma diminuição da captação periférica de glicose. A nefropatia diabética (ND), através da inflamação subclínica e do aumento no estresse oxidativo, contribui para a RI e o desenvolvimento da SM. A prevalência da SM no DM1 varia entre 12 a 40%, sendo mais freqüente nos pacientes com ND e controle glicêmico insatisfatório. Estes achados possuem implicações na terapêutica e no prognóstico cardiovascular dos pacientes com DM1.UNIFESP-EPM Departamento de MedicinaUNIFESP, EPM, Depto. de MedicinaSciELOSociedade Brasileira de Endocrinologia e MetabologiaUniversidade Federal de São Paulo (UNIFESP)Dib, Sergio Atala [UNIFESP]2015-06-14T13:32:02Z2015-06-14T13:32:02Z2006-04-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion250-263application/pdfhttp://dx.doi.org/10.1590/S0004-27302006000200011Arquivos Brasileiros de Endocrinologia & Metabologia. Sociedade Brasileira de Endocrinologia e Metabologia, v. 50, n. 2, p. 250-263, 2006.10.1590/S0004-27302006000200011S0004-27302006000200011.pdf0004-2730S0004-27302006000200011http://repositorio.unifesp.br/handle/11600/2995porArquivos Brasileiros de Endocrinologia & Metabologiainfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-04T15:29:24Zoai:repositorio.unifesp.br/:11600/2995Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-04T15:29:24Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
Insulin resistance and metabolic syndrome in type 1 diabetes mellitus
title Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
spellingShingle Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
Dib, Sergio Atala [UNIFESP]
Insulin resistance
Metabolic syndrome
Type 1 diabetes mellitus
Resistência à insulina
Síndrome metabólica
Diabetes melito do tipo 1
title_short Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
title_full Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
title_fullStr Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
title_full_unstemmed Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
title_sort Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
author Dib, Sergio Atala [UNIFESP]
author_facet Dib, Sergio Atala [UNIFESP]
author_role author
dc.contributor.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Dib, Sergio Atala [UNIFESP]
dc.subject.por.fl_str_mv Insulin resistance
Metabolic syndrome
Type 1 diabetes mellitus
Resistência à insulina
Síndrome metabólica
Diabetes melito do tipo 1
topic Insulin resistance
Metabolic syndrome
Type 1 diabetes mellitus
Resistência à insulina
Síndrome metabólica
Diabetes melito do tipo 1
description Insulin resistance (IR) plays a larger role in the type 1 diabetes mellitus (T1DM) disease process than commonly recognized. Overweight and physical inactivity have increased steadily for the last 20-30 years in children and adolescents in many populations, concurrently with a rising incidence of T1DM. The role of IR in T1DM has only recently been gaining acceptance. This review will focus on how IR influences our current understanding of disease development and metabolic syndrome (MS) in T1DM. Increases in IR by weight gain and sedentarism, associated to decreased beta cell mass by autoimmune process, may disrupt normoglycemia in pre-T1DM individuals. IR may reflect a more aggressive form of autoimmune disease mediated by immuno-inflammatory factors that also mediate beta cell destruction (TNF-alpha and IL-6). These concepts are included in the accelerator hypothesis. Moreover, family history of T2DM and chronic hyperglycemia (glucotoxicity), occurring after T1DM diagnosis, contribute to decrease peripheral glucose uptake. The onset of diabetic nephropathy (DN) might also contribute to IR and metabolic syndrome (MS) via low-grade inflammation and increased oxidative stress. MS is found between 12 to 40% in T1DM, especially in patients with advanced DN and poor glycemic control. These findings have therapeutic and cardiovascular prognostic implications as children make the transition toward adolescence and young adulthood T1DM.
publishDate 2006
dc.date.none.fl_str_mv 2006-04-01
2015-06-14T13:32:02Z
2015-06-14T13:32:02Z
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://dx.doi.org/10.1590/S0004-27302006000200011
Arquivos Brasileiros de Endocrinologia & Metabologia. Sociedade Brasileira de Endocrinologia e Metabologia, v. 50, n. 2, p. 250-263, 2006.
10.1590/S0004-27302006000200011
S0004-27302006000200011.pdf
0004-2730
S0004-27302006000200011
http://repositorio.unifesp.br/handle/11600/2995
url http://dx.doi.org/10.1590/S0004-27302006000200011
http://repositorio.unifesp.br/handle/11600/2995
identifier_str_mv Arquivos Brasileiros de Endocrinologia & Metabologia. Sociedade Brasileira de Endocrinologia e Metabologia, v. 50, n. 2, p. 250-263, 2006.
10.1590/S0004-27302006000200011
S0004-27302006000200011.pdf
0004-2730
S0004-27302006000200011
dc.language.iso.fl_str_mv por
language por
dc.relation.none.fl_str_mv Arquivos Brasileiros de Endocrinologia & Metabologia
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 250-263
application/pdf
dc.publisher.none.fl_str_mv Sociedade Brasileira de Endocrinologia e Metabologia
publisher.none.fl_str_mv Sociedade Brasileira de Endocrinologia e Metabologia
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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