Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome
The metabolic syndrome is a cluster of cardiometabolic alterations that include the presence of arterial hypertension, insulin resistance, dyslipidemia, and abdominal obesity. Obesity is associated with a chronic inflammatory response, characterized by abnormal adipokine production, and the activati...
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Wiley
2013-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2013/136584 |
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author | Eduardo Fuentes Francisco Fuentes Gemma Vilahur Lina Badimon Iván Palomo |
author_facet | Eduardo Fuentes Francisco Fuentes Gemma Vilahur Lina Badimon Iván Palomo |
author_sort | Eduardo Fuentes |
collection | DOAJ |
description | The metabolic syndrome is a cluster of cardiometabolic alterations that include the presence of arterial hypertension, insulin resistance, dyslipidemia, and abdominal obesity. Obesity is associated with a chronic inflammatory response, characterized by abnormal adipokine production, and the activation of proinflammatory signalling pathways resulting in the induction of several biological markers of inflammation. Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Adiponectin can either act directly on macrophages to shift polarization and/or prime human monocytes into alternative M2-macrophages with anti-inflammatory properties. Meanwhile, the chronic inflammation in adipose tissue is regulated by a series of transcription factors, mainly PPARs and C/EBPs, that in conjunction regulate the expression of hundreds of proteins that participate in the metabolism and storage of lipids and, as such, the secretion by adipocytes. Therefore, the management of the metabolic syndrome requires the development of new therapeutic strategies aimed to alter the main genetic pathways involved in the regulation of adipose tissue metabolism. |
format | Article |
id | doaj-art-ae9de58be8974bb6b416d065a7f213ac |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2013-01-01 |
publisher | Wiley |
record_format | Article |
series | Mediators of Inflammation |
spelling | doaj-art-ae9de58be8974bb6b416d065a7f213ac2025-02-03T01:27:27ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/136584136584Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic SyndromeEduardo Fuentes0Francisco Fuentes1Gemma Vilahur2Lina Badimon3Iván Palomo4Immunology and Haematology Laboratory, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Interdisciplinary Excellence Research Program on Healthy Aging, Universidad de Talca, Talca, ChileInterno Sexto Año, Escuela de Medicina, Facultad de Medicina, Universidad Católica del Maule, ChileCentro de Investigación Cardiovascular, ICCC-CSIC, Hospital de la Santa Creu i Sant Pau, CiberOBN, Instituto Carlos III, Barcelona, SpainCentro de Investigación Cardiovascular, ICCC-CSIC, Hospital de la Santa Creu i Sant Pau, CiberOBN, Instituto Carlos III, Barcelona, SpainImmunology and Haematology Laboratory, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Interdisciplinary Excellence Research Program on Healthy Aging, Universidad de Talca, Talca, ChileThe metabolic syndrome is a cluster of cardiometabolic alterations that include the presence of arterial hypertension, insulin resistance, dyslipidemia, and abdominal obesity. Obesity is associated with a chronic inflammatory response, characterized by abnormal adipokine production, and the activation of proinflammatory signalling pathways resulting in the induction of several biological markers of inflammation. Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Adiponectin can either act directly on macrophages to shift polarization and/or prime human monocytes into alternative M2-macrophages with anti-inflammatory properties. Meanwhile, the chronic inflammation in adipose tissue is regulated by a series of transcription factors, mainly PPARs and C/EBPs, that in conjunction regulate the expression of hundreds of proteins that participate in the metabolism and storage of lipids and, as such, the secretion by adipocytes. Therefore, the management of the metabolic syndrome requires the development of new therapeutic strategies aimed to alter the main genetic pathways involved in the regulation of adipose tissue metabolism.http://dx.doi.org/10.1155/2013/136584 |
spellingShingle | Eduardo Fuentes Francisco Fuentes Gemma Vilahur Lina Badimon Iván Palomo Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome Mediators of Inflammation |
title | Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome |
title_full | Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome |
title_fullStr | Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome |
title_full_unstemmed | Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome |
title_short | Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome |
title_sort | mechanisms of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome |
url | http://dx.doi.org/10.1155/2013/136584 |
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