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Journal of Lipid Research, Vol. 48, 751-762, April 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Review

The role of TNF- in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk

Calin Popa^*,, Mihai G. Netea^*, Piet L. C. M. van Riel, Jos W. M. van der Meer^* and Anton F. H. Stalenhoef^1,*

^* Department of General Internal Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands
Department of Rheumatology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands

Published, JLR Papers in Press, January 2, 2007.

¹ To whom correspondence should be addressed. e-mail: a.stalenhoef{at}aig.umcn.nl

The recent insight that inflammation contributes to the development of atherosclerosis and type 2 diabetes mellitus constitutes a major breakthrough in understanding the mechanisms underlying these conditions. In addition, it opens the way for new therapeutic approaches that might eventually decrease the prevalence of these public health problems. Tumor necrosis factor- (TNF-) has been shown to play a key role in these processes and thus might be a potential therapeutic target. Increased concentrations of TNF- are found in acute and chronic inflammatory conditions (e.g., trauma, sepsis, infection, rheumatoid arthritis), in which a shift toward a proatherogenic lipid profile and impaired glucose tolerance occurs. Although therapeutic blockade of TNF- worsens the prognosis in patients with abscesses and granulomatous infections, this strategy is highly beneficial in the case of chronic inflammatory conditions, including rheumatoid arthritis. Current investigations assessing the impact of anti-TNF agents on intermediary metabolism suggest that TNF- blockade may improve insulin resistance and lipid profiles in patients with chronic inflammatory diseases.

Supplementary key words tumor necrosis factor- • lipids • anti-tumor necrosis factor • insulin resistance

Abbreviations: apoA-I, apolipoprotein A-I; ATGL, adipocyte triglyceride lipase; CETP, cholesteryl ester transfer protein; CYP7A1, cholesterol-7-hydroxylase; DM, diabetes mellitus; HSL, hormone-sensitive lipase; IL-6, interleukin-6; IRS-1, insulin receptor substrate-1; JNK, c-jun-NH₂-terminal kinase; LPS, lipopolysaccharide; RA, rheumatoid arthritis; RCT, reverse cholesterol transport; TG, triglyceride; TNF-, tumor necrosis factor-; TNF-RI, tumor necrosis factor receptor type I

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