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Mediators of Inflammation
Volume 2013, Article ID 136584, 11 pages
Review Article

Mechanisms of Chronic State of Inflammation as Mediators That Link Obese Adipose Tissue and Metabolic Syndrome

1Immunology and Haematology Laboratory, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Interdisciplinary Excellence Research Program on Healthy Aging, Universidad de Talca, Talca, Chile
2Centro de Estudios en Alimentos Procesados (CEAP), Conicyt-Regional, Gore Maule, R09I2001 Talca, Chile
3Interno Sexto Año, Escuela de Medicina, Facultad de Medicina, Universidad Católica del Maule, Chile
4Centro de Investigación Cardiovascular, ICCC-CSIC, Hospital de la Santa Creu i Sant Pau, CiberOBN, Instituto Carlos III, Barcelona, Spain

Received 10 April 2013; Accepted 31 May 2013

Academic Editor: Oreste Gualillo

Copyright © 2013 Eduardo Fuentes et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.