Adipose tissue is a dynamic endocrine organ that secretes a number of factors that are increasingly recognized to contribute to systemic and vascular
inflammation. Several of these factors, collectively referred to as
adipokines, have now been shown regulate, directly or indirectly, a number of the processes that contribute to the development of
atherosclerosis, including
hypertension, endothelial dysfunction,
insulin resistance, and
vascular remodeling. Several
adipokines are preferentially expressed in visceral adipose tissue, and the secretion of proinflammatory
adipokines is elevated with increasing adiposity. Not surprisingly, approaches that reduce adipose tissue depots, including surgical fat removal, exercise, and reduced caloric intake, improve proinflammatory
adipokine levels and reduce the severity of their resultant pathologies. Systemic
adipokine levels can also be favorably altered by treatment with several of the existing
drug classes used to treat
insulin resistance,
hypertension, and
hypercholesterolemia. Greater understanding of
adipokine regulation, however, should result in the design of improved treatment strategies to control disease states associated with increase adiposity, an important outcome in view of the growing worldwide epidemic of
obesity.