TNF-α, a potent lipid metabolism regulator

被引:174
作者
Chen, Xiuping [1 ,2 ]
Xun, Keli [3 ]
Chen, Lidian [2 ]
Wang, Yitao [1 ]
机构
[1] Fujian Coll Tradit Chinese Med, Fuzhou, Peoples R China
[2] Univ Macau, Inst Chinese Med Sci, Macau, Peoples R China
[3] Peoples Hosp Binzhou, Dept Dermatol, Binzhou, Peoples R China
关键词
tumor necrosis factor alpha; free fatty acid; lipolysis; cholesterol; leptin; adiponectin; infliximab; TUMOR-NECROSIS-FACTOR; LIPOPROTEIN-LIPASE ACTIVITY; ESTER TRANSFER PROTEIN; CARBOXYLASE GENE-EXPRESSION; ADIPOSE TRIGLYCERIDE LIPASE; SIGNAL-RELATED KINASE; MESSENGER-RNA LEVELS; NF-KAPPA-B; INSULIN-RESISTANCE; CHOLESTEROL LEVELS;
D O I
10.1002/cbf.1596
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
As a multifunctional cytokine, tumor necrosis factor alpha (TNF-alpha) exerts a series of biological actions in different cells, tissues, organs, and species and has been demonstrated to regulate and interfere with energy metabolism, especially lipid homeostasis. A large body of researches suggested that the effects of TNF-alpha on lipid metabolism mainly include five aspects: ( I) Suppresses free fatty acid (FFA) uptake and promotes lipogenesis; (2) induces lipolysis; (3) inhibits lipid-metabolism-related enzymes activity, (4) regulates cholesterol metabolism; (5) regulates other adipocyte-derived adipokines. The molecular mechanisms underlying these actions are complex and several signal transduction pathways might be involved. Regulation of metabolism-related gene expression at transcriptional and protein levels and impact on enzymes activity might be of importance. Identification and verification of these pathways might provide novel potential strategies and drug targets for dyslipidemia therapy. However, the inconsistent and even conflict conclusions on lipid profile drawn from human subjects after infliximab therapy poses the possibility that the effect of TNF-alpha oil lipid metabolism might be more complicated than it appeared to be. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:407 / 416
页数:10
相关论文
共 129 条
[1]
Control of adipose tissue lipid metabolism by tumor necrosis factor-α in rainbow trout (Oncorhynchus mykiss) [J].
Albalat, A ;
Liarte, C ;
MacKenzie, S ;
Tort, L ;
Planas, JV ;
Navarro, I .
JOURNAL OF ENDOCRINOLOGY, 2005, 184 (03) :527-534
[2]
Effects of repeated infliximab therapy on serum lipid profile in patients with refractory rheumatoid arthritis [J].
Allanore, Y ;
Kahan, A ;
Sellam, J ;
Ekindjian, OG ;
Borderie, D .
CLINICA CHIMICA ACTA, 2006, 365 (1-2) :143-148
[3]
Elevated triglyceride and cholesterol levels after intravenous antitumour necrosis factor-α therapy in a patient with psoriatic arthritis and psoriasis vulgaris [J].
Antoniou, C. ;
Dessinioti, C. ;
Katsambas, A. ;
Stratigos, A. J. .
BRITISH JOURNAL OF DERMATOLOGY, 2007, 156 (05) :1090-1091
[4]
Atorvastatin reduces proinflammatory markers in hypercholesterolemic patients [J].
Ascer, E ;
Bertolami, MC ;
Venturinelli, ML ;
Buccheri, V ;
Souza, J ;
Nicolau, JC ;
Ramires, JAF ;
Serrano, CV .
ATHEROSCLEROSIS, 2004, 177 (01) :161-166
[5]
Targeting cholesteryl ester transfer protein for the prevention and management of cardiovascular disease [J].
Barter, PJ ;
Kastelein, JJP .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2006, 47 (03) :492-499
[6]
SUPPRESSION OF PEROXISOMAL LIPID BETA-OXIDATION ENZYMES BY TNF-ALPHA [J].
BEIER, K ;
VOLKL, A ;
FAHIMI, HD .
FEBS LETTERS, 1992, 310 (03) :273-276
[7]
Beltowski Jerzy, 2008, Cardiovascular & Hematological Disorders - Drug Targets, V8, P7, DOI 10.2174/187152908783884920
[8]
Free fatty acids produce insulin resistance and activate the proinflammatory nuclear factor-κB pathway in rat liver [J].
Boden, G ;
She, PX ;
Mozzoli, M ;
Cheung, P ;
Gumireddy, K ;
Reddy, P ;
Xiang, XQ ;
Luo, ZJ ;
Ruderman, N .
DIABETES, 2005, 54 (12) :3458-3465
[9]
ENDOTOXIN-INDUCED SERUM FACTOR THAT CAUSES NECROSIS OF TUMORS [J].
CARSWELL, EA ;
OLD, LJ ;
KASSEL, RL ;
GREEN, S ;
FIORE, N ;
WILLIAMSON, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1975, 72 (09) :3666-3670
[10]
Cauza E, 2002, WIEN KLIN WOCHENSCHR, V114, P1004