Resistin and visfatin: regulators of insulin sensitivity, inflammation and immunity

Abstract

Adipokines play a significant role in the pathogenesis of a low-grade inflammation associated with obesity and metabolic syndrome, and in chronic inflammatory and autoimmune diseases such as rheumatoid arthritis. Among variety of adipokines, resistin and visfatin are proposed as important pro-inflammatory mediators, which also interfere with the central regulation of insulin sensitivity. Resistin has been initially postulated as a risk factor for insulin resistance, however, the subsequent available data on it have revealed contradictory findings in both humans and rodents. On the other hand, visfatin has been suggested to be a beneficial adipokine with insulin-mimicking/-sensitizing effects, but regulation of visfatin production and its physiological importance in the conditions of obesity and type 2 diabetes mellitus are still not completely understood. Despite the opposing effects of resistin and visfatin on the regulation of insulin sensitivity, both adipokines have pro-inflammatory properties. Clinical and experimental studies have shown that the expression and secretion of resistin and visfatin are up-regulated during inflammation and in response to pro-inflammatory cytokines. It has also become increasingly evident that resistin as well as visfatin itself can contribute to the inflammatory processes by triggering cytokine production and NF-kappaB activation. New insight into the role of adipokines makes them attractive targets for novel therapeutic strategies in chronic inflammatory diseases or subclinical inflammation relating to obesity and various metabolic abnormalities.