RESUMO
The metabolic syndrome (MetS) is a cluster of clinical disorders including an unhealthy body habitus with a large waistline, dyslipidemia, glucose intolerance and hypertension. It is known that these disorders not only increase the chances of developing type 2 diabetes mellitus (T2DM), but also cardiovascular disease (CVD). Furthermore, the co-occurrence of all these risk factors known as the MetS is linked to pathways sharing common underlying mediators and mechanisms. Though insulin resistance has been considered as the root of the problem to explain the conglomerate of metabolic abnormalities within this syndrome; new evidence points to several pro-inflammatory cytokines, reactive oxygen species and free fatty acid intermediates might play an even greater role in regulating a series of intracellular signaling pathways sustain as well as perpetuate the development of the MetS and its CVD complications. Since having a diagnosis of MetS confers not only a 5-fold increase in the risk of T2DM, but also a 2-fold risk of developing CVD over a period of 5 to 10 years; it is vital to better recognize the mechanisms by which the MetS is associated with such adverse outcomes. Therefore, it is the purpose of this review to address (1) how inflammation modifies insulin sensitivity, (2) known factors believed to contribute to this process, and (3) new concepts of inflammatory markers in regulating the development of MetS and its individual components.