Chronic inflammation has recently been proposed to be a key mediator linking obesity to a cluster of cardiometabolic disorders. Obese adipose tissue, infiltrated with activated macrophages and mast cells, is an important source of systemic inflammation, by secreting dozens of the pro-inflammatory adipokines into the blood stream. One the other hand, adiponectin, an abundant adipokine secreted predominantly from adipocytes, is markedly decreased in obesity and associated inflammatory diseases. Adiponectin exerts its anti-inflammatory actions in several target cells by inhibiting the production and activities of tumor necrosis factor-alpha, preventing the activation of nuclear factor-kappa B, and inducing expression of anti-inflammatory cytokines. In animal models, adiponectin treatment alleviates several obesity-associated inflammatory diseases, such as atherosclerosis, nonalcoholic steatohepatitis, asthma and acute myocardial infarction. In humans, circulating levels of adiponectin are inversely correlated with several well-established markers of inflammation, including C-reactive protein and interleukin-6. Furthermore, anti-inflammatory drugs, such as peroxisome proliferator-activated receptor-gamma agonists, can elevate plasma levels of adiponectin. While the majority of clinical and animal data support the role of adiponectin as an anti-inflammatory, anti-atheroscerotic and anti-diabetic adipokine, a number of recent studies have reported its pro-inflammatory actions in certain conditions. Here, we summarize the pathophysiological roles of adiponectin in inflammation-related disorders, and discuss the potential mechanisms involved, also their implications in adiponectin-targeted pharmacotherapy.
Biomedical Reviews 2006, 17: 11-22.
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