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Implication of inflammatory signaling pathways in obesity-induced insulin resistance
Obesity is characterized by the development of a low-grade chronic inflammatory state in different metabolic tissues including adipose tissue and liver. This inflammation develops in response to an excess of nutrient flux and is now recognized as an important link between obesity and insulin resista...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539134/ https://www.ncbi.nlm.nih.gov/pubmed/23316186 http://dx.doi.org/10.3389/fendo.2012.00181 |
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author | Tanti, Jean-François Ceppo, Franck Jager, Jennifer Berthou, Flavien |
author_facet | Tanti, Jean-François Ceppo, Franck Jager, Jennifer Berthou, Flavien |
author_sort | Tanti, Jean-François |
collection | PubMed |
description | Obesity is characterized by the development of a low-grade chronic inflammatory state in different metabolic tissues including adipose tissue and liver. This inflammation develops in response to an excess of nutrient flux and is now recognized as an important link between obesity and insulin resistance. Several dietary factors like saturated fatty acids and glucose as well as changes in gut microbiota have been proposed as triggers of this metabolic inflammation through the activation of pattern-recognition receptors (PRRs), including Toll-like receptors (TLR), inflammasome, and nucleotide oligomerization domain (NOD). The consequences are the production of pro-inflammatory cytokines and the recruitment of immune cells such as macrophages and T lymphocytes in metabolic tissues. Inflammatory cytokines activate several kinases like IKKβ, mTOR/S6 kinase, and MAP kinases as well as SOCS proteins that interfere with insulin signaling and action in adipocytes and hepatocytes. In this review, we summarize recent studies demonstrating that PRRs and stress kinases are important integrators of metabolic and inflammatory stress signals in metabolic tissues leading to peripheral and central insulin resistance and metabolic dysfunction. We discuss recent data obtained with genetically modified mice and pharmacological approaches suggesting that these inflammatory pathways are potential novel pharmacological targets for the management of obesity-associated insulin resistance. |
format | Online Article Text |
id | pubmed-3539134 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-35391342013-01-11 Implication of inflammatory signaling pathways in obesity-induced insulin resistance Tanti, Jean-François Ceppo, Franck Jager, Jennifer Berthou, Flavien Front Endocrinol (Lausanne) Endocrinology Obesity is characterized by the development of a low-grade chronic inflammatory state in different metabolic tissues including adipose tissue and liver. This inflammation develops in response to an excess of nutrient flux and is now recognized as an important link between obesity and insulin resistance. Several dietary factors like saturated fatty acids and glucose as well as changes in gut microbiota have been proposed as triggers of this metabolic inflammation through the activation of pattern-recognition receptors (PRRs), including Toll-like receptors (TLR), inflammasome, and nucleotide oligomerization domain (NOD). The consequences are the production of pro-inflammatory cytokines and the recruitment of immune cells such as macrophages and T lymphocytes in metabolic tissues. Inflammatory cytokines activate several kinases like IKKβ, mTOR/S6 kinase, and MAP kinases as well as SOCS proteins that interfere with insulin signaling and action in adipocytes and hepatocytes. In this review, we summarize recent studies demonstrating that PRRs and stress kinases are important integrators of metabolic and inflammatory stress signals in metabolic tissues leading to peripheral and central insulin resistance and metabolic dysfunction. We discuss recent data obtained with genetically modified mice and pharmacological approaches suggesting that these inflammatory pathways are potential novel pharmacological targets for the management of obesity-associated insulin resistance. Frontiers Media S.A. 2013-01-08 /pmc/articles/PMC3539134/ /pubmed/23316186 http://dx.doi.org/10.3389/fendo.2012.00181 Text en Copyright © 2013 Tanti, Ceppo, Jager and Berthou. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc. |
spellingShingle | Endocrinology Tanti, Jean-François Ceppo, Franck Jager, Jennifer Berthou, Flavien Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title | Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title_full | Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title_fullStr | Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title_full_unstemmed | Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title_short | Implication of inflammatory signaling pathways in obesity-induced insulin resistance |
title_sort | implication of inflammatory signaling pathways in obesity-induced insulin resistance |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539134/ https://www.ncbi.nlm.nih.gov/pubmed/23316186 http://dx.doi.org/10.3389/fendo.2012.00181 |
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