Abstract
The traditional view of the adipocyte as a passive receptacle for storage and combustion of triacylglycerol is undergoing rapid change. It is now recognized that a variety of adipocyte and adipose stromal cell derived bioactive peptides, collectively termed “adipokines”, act both locally and distally through autocrine, paracrine and endocrine effects. Alteration of adipose tissue mass in obesity increases the production of most adipose secreted factors; therefore white adipose tissue could play a key role in multiple metabolic disorders and in the increased risk of cardiovascular disease associated with obesity. In fact, increased activity of tumor necrosis factor and interleukin 6 are involved in the development of the insulin resistance present in obesity. In contrast, other adipokines, like adiponectin and leptin, are insulin sparing through stimulatory affects on the beta oxidation of fatty acids in skeletal muscle. Other adipokine have been implicated in hypertension (angiotensinogen) and impaired fibrinolysis (PAI-1). The role of resistin is poorly understood: this protein seems surely implicated in insulin resistance in rats, but probably not in humans. Reduction of adipose tissue mass, through weight reduction in association with exercise, has been shown to improve the adipokines production (reduction in TNF-α and IL-6, increase in adiponectin) while the thiazolinedione drugs increase endogenous adiponectin production. These results support the idea that the development of new drug targeting adipokines might represent a promising therapeutic approach to protect obese patients from atherosclerosis. This paper will review the function and the regulation of adipocytokines in order to understand how obesity may contribute to metabolic syndrome.
Keywords: adipokines, atherosclerosis, inflammation
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