Supplementation with ω3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers

被引:67
作者
Vega-López, S [1 ]
Kaul, N [1 ]
Devaraj, S [1 ]
Cai, RY [1 ]
German, B [1 ]
Jialal, I [1 ]
机构
[1] Univ Calif Davis, Lab Atherosclerosis & Metab Res, Med Ctr, Sacramento, CA 95817 USA
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2004年 / 53卷 / 02期
关键词
D O I
10.1016/j.metabol.2003.09.012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
There is growing evidence supporting the importance of inflammation in all stages of atherosclerosis. While both omega-3 polyunsaturated fatty acids (n3PUFA) and the lipid-soluble antioxidant alpha-tocopherol (AT) have been shown to independently have significant anti-inflammatory effects, there is paucity of data examining the effect of n3PUFA alone and in combination with AT on markers of inflammation and monocyte function. Therefore, we tested the effect of n3PUFA alone, all-rac (synthetic) AT alone, and the combination on markers of inflammation and monocyte function. Healthy nonsmoking volunteers were randomly assigned to 1 of 4 groups (n = 20 per group): 1.5 g/d n3PUFA, 800 IU/d AT, 1.5 g n3PUFA + 800 IU/d AT, or placebo in a parallel double-blinded study. Compared to baseline, 12 weeks of supplementation resulted in no changes in plasma lipids regardless of treatment. Plasma AT was significantly increased only in those groups that received AT (P < .0001). Similarly, groups receiving n3PUFA showed a significant increase in plasma docosahexaenoic acid (P < .0001). No significant within- or between-group differences were found for plasma levels of high-sensitivity C-reactive protein (hsCRP). Furthermore, there were no differences in monocyte proinflammatory cytokine release (interleukin [IL]-1beta, tumor necrosis factor [TNF]-alpha and IL-6) after activation with monocyte chemotactic protein-1 (MCP-1). In conclusion, supplementation with n3PUFA and all-rac AT at these doses is not anti-inflammatory. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:236 / 240
页数:5
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