Published online Jun 15, 2014. doi: 10.4239/wjd.v5.i3.357
Revised: April 14, 2014
Accepted: May 15, 2014
Published online: June 15, 2014
The traditional perception of adipose tissue as a storage organ of fatty acids has been replaced by the notion that adipose tissue is an active endocrine organ, releasing various adipokines that are involved in the pathogenesis of obesity-related metabolic disturbances. Obesity is a well-known risk factor for atherosclerosis, and accelerates atherosclerosis by many mechanisms such as increase in blood pressure and glucose level, abnormal lipid profiles, and systemic inflammation. Furthermore, growing evidence suggests that some adipokines directly mediate the process of atherosclerosis by influencing the function of endothelial cells, arterial smooth muscle cells, and macrophages in vessel walls. In obese patients, the secretion and coordination of such adipokines is abnormal, and the secretion of specific adipokines increases or decreases. Accordingly, the discovery of new adipokines and elucidation of their functions might lead to a new treatment strategy for metabolic disorders related to obesity, including cardiovascular diseases.
Core tip: This review summarizes recent laboratory and clinical studies on the influence of various adipokines, including adiponectin, resistin, adipocyte fatty acid binding protein, omentin-1, and chemerin, on the development of atherosclerosis.