The Concept of CMR

Obesity and inflammation

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Obesity is a chronic, low-grade inflammatory state, as demonstrated by increased levels of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) and acute phase proteins such as C-reactive protein (CRP) (26). Weight loss has a positive impact on this pro-inflammatory state (27). In addition to its direct effects, inflammation may cause thrombosis indirectly by inducing oxidative stress and endothelial dysfunction (28). IL-6 may promote thrombosis indirectly by increasing platelet count and aggregation, hepatic synthesis of fibrinogen and CRP, and endothelial adhesion molecule expression, as well as by decreasing adiponectin secretion (29). TNF-α stimulates leptin production and reduces adiponectin secretion by adipose tissue, induces PAI-1 expression in adipose tissue, and promotes endothelial adhesion molecule expression (7) (Figure).

Reference

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7. Kershaw EE and Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004; 89: 2548-56.

26. Yudkin JS, Stehouwer CD, Emeis JJ, et al. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19: 972-8.

27. Ziccardi P, Nappo F, Giugliano G, et al. Reduction of inflammatory cytokine concentrations and improvement of endothelial functions in obese women after weight loss over one year. Circulation 2002; 105: 804-9.

28. Sonnenberg GE, Krakower GR and Kissebah AH. A novel pathway to the manifestations of metabolic syndrome. Obes Res 2004; 12: 180-6.

29. Woods A, Brull DJ, Humphries SE, et al. Genetics of inflammation and risk of coronary artery disease: the central role of interleukin-6. Eur Heart J 2000; 21: 1574-83.

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