Adipose tissue dysfunction and inflammation in cardiovascular disease.

Abstract

Adipose tissue (AT) was long perceived as a passive lipid storage depot but it is now considered as an endocrine organ that produces a large number of mediators that affect metabolism, inflammation and coagulation. In obesity, the increased size of adipocytes and chronic low-grade inflammation within AT alter its normal physiological function. AT dysfunction results in altered production and secretion of adipokines, which in turn affect several tissues, e.g. the liver, skeletal muscles and vasculature, in a para- or endocrine manner. Numerous circulating proinflammatory mediators involved in the development of cardiovascular disease (CVD) are directly released from adipocytes, thereby linking obesity to an increased cardiovascular risk. In the current chapter, we focus, on the one hand, on a small selection of novel adipokines with a potentially strong link to CVD: soluble dipeptidyl peptidase-4, visfatin and lipocalin-2. On the other hand, we summarize the most recent findings on the novel cardioprotective adipokines omentin and apelin.