Metabolic syndrome is an inflammatory disorder: A conspiracy between adipose tissue and phagocytes.

Metabolic syndrome (MetS) describes a cluster of cardio-metabolic factors that predispose to type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease (ASCVD). While 35% of Americans suffer from this disorder, the specific pathways related to this disease are largely underexplored. The prevailing consensus is that inflammatory pathways contribute to the pathogenesis of this disease, and therefore new research has uncovered how inflammation plays a critical role in the development and progression of MetS. The purpose of this review is to understand the role of major inflammatory mechanisms and their role in MetS. Our review identifies that adipose tissue (AT) contributes to the inflammatory pathways through the release of pro-inflammatory adipokines such as leptin and chemerin and dysregulation of anti-inflammatory adiponectin. Chemokines and cytokines deriving from monocytes are also altered and promote inflammation and insulin resistance. Circulating inflammatory biomarkers including C-reactive protein (CRP), fibrinogen, Serum amyloid A (SAA), cytokines, and chemokines have also been linked to the pathogenesis of MetS. Researchers have identified the significance of CRP levels in predicting future sequelae of MetS such as ASCVD. Mast cells in subcutaneous adipose tissue (SAT) promote both inflammation and fibrosis. Thus, both AT and phagocyte activity define MetS as an inflammatory disorder.