N-3 polyunsaturated fatty acids regulate lipid metabolism through several inflammation mediators: mechanisms and implications for obesity prevention

被引:90
作者
Tai, Chen C. [1 ]
Ding, Shih T. [1 ]
机构
[1] Natl Taiwan Univ, Dept Anim Sci, Ctr Biotechnol, Taipei 106, Taiwan
关键词
Docosahexaenoic acid; Inflammation; Interleukin-6; Obesity; n-3; PUFA; Serum amyloid A; Tumor necrosis factor-alpha; TUMOR-NECROSIS-FACTOR; SERUM-AMYLOID-A; NF-KAPPA-B; HORMONE-SENSITIVE LIPASE; INDUCED INSULIN-RESISTANCE; ELEMENT-BINDING PROTEIN-1; DIFFERENTIATION-DEPENDENT FACTOR-1; RESIDENT PERITONEAL-MACROPHAGES; FISH-OIL SUPPLEMENTATION; ALPHA-INDUCED LIPOLYSIS;
D O I
10.1016/j.jnutbio.2009.09.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Obesity is a growing problem that threatens the health and welfare of a large proportion of the human population. The n-3 polyunsaturated fatty acids (PUFA) are dietary factors that have potential to facilitate reduction in body fat deposition and improve obesity-induced metabolic syndromes. The n-3 PUFA up-regulate several inflammation molecules including serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in hepatocytes and adipocytes. Actions of these inflammation mediators resemble those of n-3 PUFA in the modulation of many lipid metabolism-related genes. For instance, they both suppress expressions of perilipin, sterol regulatory element binding protein-1 (SREBP-1) and lipoprotein lipase (LPL) to induce lipolysis and reduce lipogenesis. This review will connect these direct or indirect regulating pathways between n-3 PUFA, inflammation mediators, lipid metabolism-related genes and body fat reduction. A thorough knowledge of these regulatory mechanisms will lead us to better utilization of n-3 PUFA to reduce lipid deposition in the liver and other tissues, therefore presenting an opportunity for developing new strategies to treat obesity. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:357 / 363
页数:7
相关论文
共 120 条
[1]  
Abbas A.K., 2007, CELLULAR MOL IMMUNOL
[2]   Dietary eicosapentaenoic acid and docosahexaenoic acid are more effective than alpha-linolenic acid in improving insulin sensitivity in rats [J].
Andersen, Gaby ;
Harnack, Kerstin ;
Erbersdobler, Helmut F. ;
Somoza, Veronika .
ANNALS OF NUTRITION AND METABOLISM, 2008, 52 (03) :250-256
[3]   Identification of novel phosphorylation sites in hormone-sensitive lipase that are phosphorylated in response to isoproterenol and govern activation properties in vitro [J].
Anthonsen, MW ;
Rönnstrand, L ;
Wernstedt, C ;
Degerman, E ;
Holm, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (01) :215-221
[4]   FUNCTION AMD ACTIVATION OF NF-KAPPA-B IN THE IMMUNE-SYSTEM [J].
BAEUERLE, PA ;
HENKEL, T .
ANNUAL REVIEW OF IMMUNOLOGY, 1994, 12 :141-179
[5]   LIPOPROTEIN-LIPASE IN RATS FED FISH OIL - APPARENT RELATIONSHIP TO PLASMA-INSULIN LEVELS [J].
BALTZELL, JK ;
WOOTEN, JT ;
OTTO, DA .
LIPIDS, 1991, 26 (04) :289-294
[6]   Eicosapentaenoic acid modulates the immune response but has no effect on a mimic of antigen-specific responses [J].
Barber, MD ;
Fearon, KCH ;
Ross, JA .
NUTRITION, 2005, 21 (05) :588-593
[7]   Adipose tissue IL-6 content correlates with resistance to insulin activation of glucose uptake both in vivo and in vitro [J].
Bastard, JP ;
Maachi, M ;
Van Nhieu, JT ;
Jardel, C ;
Bruckert, E ;
Grimaldi, A ;
Robert, JJ ;
Capeau, J ;
Hainque, B .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (05) :2084-2089
[8]   Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss [J].
Bastard, JP ;
Jardel, C ;
Bruckert, E ;
Blondy, P ;
Capeau, J ;
Laville, M ;
Vidal, H ;
Hainque, B .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (09) :3338-3342
[9]   Docosahexaneoic acid (22:6, n-3) regulates rat hepatocyte SREBP-1 nuclear abundance by Erk- and 26S proteasome-dependent pathways [J].
Botolin, D ;
Wang, Y ;
Christian, B ;
Jump, DB .
JOURNAL OF LIPID RESEARCH, 2006, 47 (01) :181-192
[10]   Dietary fatty acids differentially regulate production of TNF-α and IL-10 by murine 3T3-L1 adipocytes [J].
Bradley, Richard L. ;
Fisher, FFolliott M. ;
Maratos-Flier, Eleftheria .
OBESITY, 2008, 16 (05) :938-944