Among the rapidly expanding list of factors synthesized and released by white adipose tissue, the range of cytokines, chemokines and other signaling proteins, collectively termed adipokines, are of particular interest to better understand the pathogenesis of low-grade systemic inflammation associated with obesity. An overwhelming body of evidence further links high circulating concentrations of inflammatory biomarkers with the development of insulin resistance and the progression to type 2 diabetes mellitus. The secretory pattern of adipose tissue characteristic of obesity comprises an increase in pro-inflammatory adipokines together with a decrease in adipokines with anti-inflammatory, cardioprotective and insulin sensitizing actions. These molecules exerts local autocrine and paracrine effects on white adipose tissue physiology at the same time as having systemic effects on other organs. A number of factors derived not only from adipocytes but also from infiltrated macrophages and mast cells, which have been shown to accompany morbid adiposity, further contribute to inflammation and insulin resistance. The evolving notion of adipose tissue as an immuno-modulatory organ together with the improving knowledge of how inflammation exerts a (counter)regulatory action on glucose and lipid metabolism are opening up new therapeutic opportunities for applying anti-inflammatory strategies to counterbalance the detrimental consequences of excess adiposity and its comorbidities.
Biomedical Reviews 2006; 17: 43-51.
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