ABSTRACT
The hypothesis that low grade chronic systemic inflammation involving adipocytederived factors links obesity to clinical metabolic disorders is attracting growing support. Observational and experimental models of obesity have revealed that significant amounts of pro-inflammatory mediators are synthesized and secreted by adipose tissue. It is hypothesized that the release of pro-inflammatory adipokines and the cessation of synthesis of normally anti-inflammatory mediators may be caused by adipocyte hypertrophy or hyperplasia that promotes local hypoxia and cellular stress (de Luca and Olefsky, 2008).
