ABSTRACT
Perhaps the principal conclusion to be drawn from Adipose Tissue and Inflammation is that adipose tissue functions as an essential endocrine organ that produces and secretes an identifiable set of specific adipokines and that this adipokine production and secretion arise from varying physiologic and pathologic states. In states of obesity, the production profile of these adipokines is altered to one that promotes lowgrade systemic inflammation. Recent research implicates overnutrition and obesity as inducers of inflammatory responses in adipose and peripheral tissues, causing or contributing to those metabolic defects that underlie type 2 diabetes, hypertension, and cardiovascular diseases.
