Effect of weight loss on neutrophil resolvins in the metabolic syndrome

被引:27
作者
Barden, A. [1 ]
Shinde, S. [1 ]
Tsai, I-J [1 ]
Crof, K. D. [2 ]
Beilin, L. J. [1 ]
Puddey, I. B. [1 ]
Mori, T. A. [1 ]
机构
[1] Univ Western Australia, Med Sch, Perth, WA, Australia
[2] Univ Western Australia, Sch Biomed Sci, Perth, WA, Australia
来源
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2019年 / 148卷
关键词
Weight loss; Metabolic syndrome; Resolvins; Neutrophils; ACUTE-INFLAMMATION; PRORESOLVING MEDIATORS; LIPID MEDIATORS; OBESITY; RESOLUTION; SUPPLEMENTATION; EXPRESSION; PRESSURE; ALPHA; D1;
D O I
10.1016/j.plefa.2019.07.001
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
Background: Non-resolving inflammation associates with obesity and insulin resistance, and may be dependent on the balance of inflammatory substances and specialised pro-resolving mediators of inflammation (SPM) that act to halt the inflammatory response. This controlled trial examined the effect of weight loss on neutrophil synthesis of SPM in volunteers with the metabolic syndrome (MetS). Methods: Volunteers with MetS (n = 42) were matched for age and gender and randomly assigned to a 12-wk weight loss program followed by 4-wk weight stabilization or a 16-wk weight maintenance program. At baseline and 16 weeks, isolated neutrophils were stimulated with calcium ionophore and the released SPM were measured by LC-MS/MS. Results: At baseline the SPM resolvin (Rv) E1, 18R-RvE3, RvD2 and Maresin-1 (MaR-1) were detected from stimulated neutrophils. The concentration of released RvE1 was at least 6-fold that of other detected SPM. Weight loss of 4.7 +/- 0.8 kg, led to a 2-fold increase in RvE1, P = 0.013, relative to the weight maintenance group. The increase in RvE1 after weight loss was related to, but independent of leukotriene B-4. Concision: Following weight loss, human neutrophils from individuals with the metabolic syndrome are capable of releasing larger amounts of RvE1 upon stimulation.
引用
收藏
页码:25 / 29
页数:5
相关论文
共 39 条
[1]   Resolvin E1 selectively interacts with leukotriene B4 receptor BLT1 and ChemR23 to regulate inflammation [J].
Arita, Makoto ;
Ohira, Taisuke ;
Sun, Yee-Ping ;
Elangovan, Siva ;
Chiang, Nan ;
Serhan, Charles N. .
JOURNAL OF IMMUNOLOGY, 2007, 178 (06) :3912-3917
[2]   Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation [J].
Barden, Anne ;
Mas, Emilie ;
Croft, Kevin D. ;
Phillips, Michael ;
Mori, Trevor A. .
JOURNAL OF LIPID RESEARCH, 2014, 55 (11) :2401-2407
[3]   The effect of n-3 fatty acids and coenzyme Q10 supplementation on neutrophil leukotrienes, mediators of inflammation resolution and myeloperoxidase in chronic kidney disease [J].
Barden, Anne E. ;
Shinde, Sujata ;
Burke, Valerie ;
Puddey, Ian B. ;
Beilin, Lawrence J. ;
Irish, Ashley B. ;
Watts, Gerald F. ;
A. Mori, Trevor .
PROSTAGLANDINS & OTHER LIPID MEDIATORS, 2018, 136 :1-8
[4]   Weight loss is a critical factor to reduce inflammation [J].
Bianchi, Vittorio Emanuele .
CLINICAL NUTRITION ESPEN, 2018, 28 :21-35
[5]  
BOYUM A, 1984, METHOD ENZYMOL, V108, P88
[6]   Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23 [J].
Cash, Jenna L. ;
Bena, Stefania ;
Headland, Sarah E. ;
McArthur, Simon ;
Brancaleone, Vincenzo ;
Perretti, Mauro .
EMBO REPORTS, 2013, 14 (11) :999-1007
[7]   Omega-6 docosapentaenoic acid-derived resolvins and 17-hydroxydocosahexaenoic acid modulate macrophage function and alleviate experimental colitis [J].
Chiu, Cheng-Ying ;
Gomolka, Beate ;
Dierkes, Cordula ;
Huang, Nora R. ;
Schroeder, Maik ;
Purschke, Martin ;
Manstein, Dieter ;
Dangi, Bindi ;
Weylandt, Karsten H. .
INFLAMMATION RESEARCH, 2012, 61 (09) :967-976
[8]  
Crouch M.J., 2018, J. Leukoc. Biol, P1
[9]   Maresin Biosynthesis and Identification of Maresin 2, a New Anti-Inflammatory and Pro-Resolving Mediator from Human Macrophages [J].
Deng, Bin ;
Wang, Chin-Wei ;
Arnardottir, Hildur H. ;
Li, Yongsheng ;
Cheng, Chien-Yee Cindy ;
Dalli, Jesmond ;
Serhan, Charles N. .
PLOS ONE, 2014, 9 (07)
[10]   18-HEPE, an n-3 fatty acid metabolite released by macrophages, prevents pressure overload-induced maladaptive cardiac remodeling [J].
Endo, Jin ;
Sano, Motoaki ;
Isobe, Yosuke ;
Fukuda, Keiichi ;
Kang, Jing X. ;
Arai, Hiroyuki ;
Arita, Makoto .
JOURNAL OF EXPERIMENTAL MEDICINE, 2014, 211 (08) :1673-1687