Resistência à insulina e síndrome metabólica no diabetes melito do tipo 1
Autor(a) principal: | |
---|---|
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. |
id |
UFSP_558e7602af2ab6e5d3e2d00505638937 |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br/:11600/2995 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
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 |
_version_ |
1814268340616560640 |