|
 |
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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
* 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
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Lei, Y. Xiong, J. Chen, J.-B. Yang, Y. Wang, X.-Y. Yang, C. C. Y. Chang, B.-L. Song, T.-Y. Chang, and B.-L. Li TNF-alpha stimulates the ACAT1 expression in differentiating monocytes to promote the CE-laden cell formation J. Lipid Res., June 1, 2009; 50(6): 1057 - 1067. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C Popa, L J H van Tits, P Barrera, H L M Lemmers, F H J van den Hoogen, P L C M van Riel, T R D J Radstake, M G Netea, M Roest, and A F H Stalenhoef Anti-inflammatory therapy with tumour necrosis factor alpha inhibitors improves high-density lipoprotein cholesterol antioxidative capacity in rheumatoid arthritis patients Ann Rheum Dis, June 1, 2009; 68(6): 868 - 872. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Dol-Gleizes, R. Paumelle, V. Visentin, A.-M. Mares, P. Desitter, N. Hennuyer, A. Gilde, B. Staels, P. Schaeffer, and F. Bono Rimonabant, a Selective Cannabinoid CB1 Receptor Antagonist, Inhibits Atherosclerosis in LDL Receptor-Deficient Mice Arterioscler. Thromb. Vasc. Biol., January 1, 2009; 29(1): 12 - 18. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Montecucco and F. Mach Common inflammatory mediators orchestrate pathophysiological processes in rheumatoid arthritis and atherosclerosis Rheumatology, January 1, 2009; 48(1): 11 - 22. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Yu, J. Becnel, M. Zerfaoui, R. Rohatgi, A. H. Boulares, and C. D. Nichols Serotonin 5-Hydroxytryptamine2A Receptor Activation Suppresses Tumor Necrosis Factor-{alpha}-Induced Inflammation with Extraordinary Potency J. Pharmacol. Exp. Ther., November 1, 2008; 327(2): 316 - 323. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Akirav, J. A. Kushner, and K. C. Herold {beta}-Cell Mass and Type 1 Diabetes: Going, Going, Gone? Diabetes, November 1, 2008; 57(11): 2883 - 2888. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. D. Lamon and D. P. Hajjar Inflammation at the Molecular Interface of Atherogenesis: An Anthropological Journey Am. J. Pathol., November 1, 2008; 173(5): 1253 - 1264. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Egert, S. Wolffram, A. Bosy-Westphal, C. Boesch-Saadatmandi, A. E. Wagner, J. Frank, G. Rimbach, and M. J. Mueller Daily Quercetin Supplementation Dose-Dependently Increases Plasma Quercetin Concentrations in Healthy Humans J. Nutr., September 1, 2008; 138(9): 1615 - 1621. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Bartolome, B. Arteta, M. J. Martinez, Y. Chico, and B. Ochoa Kupffer cell products and interleukin 1? directly promote VLDL secretion and apoB mRNA up-regulation in rodent hepatocytes Innate Immunity, August 1, 2008; 14(4): 255 - 266. [Abstract] [PDF]
|
|
|
|
 |
|
 H. G. Kim, J. Y. Kim, M. G. Gim, J. M. Lee, and D. K. Chung Mechanical stress induces tumor necrosis factor-{alpha} production through Ca2+ release-dependent TLR2 signaling Am J Physiol Cell Physiol, August 1, 2008; 295(2): C432 - C439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. L. Oke and K. J. Tracey From CNI-1493 to the immunological homunculus: physiology of the inflammatory reflex J. Leukoc. Biol., March 1, 2008; 83(3): 512 - 517. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Di Comite and C. M. Rossi Risk of Diabetes in Patients With Rheumatoid Arthritis Taking Hydroxychloroquine JAMA, November 28, 2007; 298(20): 2368 - 2369. [Full Text] [PDF]
|
|
|
|
|
|
C. Popa, F. H J van den Hoogen, T. R D J Radstake, M. G Netea, A. E Eijsbouts, M. d. Heijer, J. W M van der Meer, P. L C M van Riel, A. F H Stalenhoef, and P. Barrera Modulation of lipoprotein plasma concentrations during long-term anti-TNF therapy in patients with active rheumatoid arthritis Ann Rheum Dis, November 1, 2007; 66(11): 1503 - 1507. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |