Grytten Elise, Laupsa-Borge Johnny, Cetin Kaya, Bohov Pavol, Nordrehaug Jan Erik, Skorve Jon, Berge Rolf K, Strand Elin, Bjørndal Bodil, Nygård Ottar K, Rostrup Espen, Mellgren Gunnar, Dankel Simon N
Hormone Laboratory, Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, Bergen, Norway; Mohn Nutrition Research Laboratory, Department of Clinical Science, University of Bergen, Bergen, Norway.
Hormone Laboratory, Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, Bergen, Norway; Mohn Nutrition Research Laboratory, Department of Clinical Science, University of Bergen, Bergen, Norway; Bevital AS, Bergen, Norway.
J Lipid Res. 2025 Apr;66(4):100770. doi: 10.1016/j.jlr.2025.100770. Epub 2025 Mar 8.
Omega-3 (n-3) (e.g., EPA/DHA) and omega-6 (n-6) (e.g., linoleic acid [LA]) FAs are suggested to have opposite effects on inflammation, but results are inconsistent and direct comparisons of n-3 and n-6 are lacking. In a double-blind, randomized, and crossover study, females (n = 16) and males (n = 23) aged 30-70 years with abdominal obesity were supplemented with 3-4 g/d EPA/DHA (fish oil) or 15-20 g/d LA (safflower oil) for 7 weeks, with a 9-week washout phase. Cytokines and chemokines (multiplex assay), acute-phase proteins (MALDI-TOF mass spectrometry), endothelial function (vascular reaction index), blood pressure, FA composition (red blood cell membranes/serum/adipose tissue, GC-MS/MS), and adipose gene expression (microarrays, quantitative PCR) were measured. While significant differences between treatments in relative change scores were found for systolic blood pressure (n-3 vs. n-6: -1.81% vs. 2.61%, P = 0.003), no differences between n-3 and n-6 were found for any circulatory inflammatory markers. However, compared with baseline, n-3 was followed by reductions in circulating TNF (-24.9%, P < 0.001), regulated upon activation, normal T cell expressed and secreted (-12.1%, P < 0.001), and macrophage inflammatory protein 1-beta (-12.5%, P = 0.014), and n-6 by lowered TNF (-18.8%, P < 0.001), regulated upon activation, normal T cell expressed and secreted (-7.37%, P = 0.027), monocyte chemoattractant protein-1 (-7.81%, P = 0.020), and macrophage inflammatory protein 1-beta (-14.2%, P = 0.010). Adipose tissue showed significant treatment differences in weight percent of EPA (n-3 vs. n-6: 50.2%∗ vs. -1.38%, P < 0.001, ∗: significant within-treatment change score), DHA (16.0%∗ vs. -3.67%, P < 0.001), and LA (-0.033 vs. 4.91%∗, P < 0.001). Adipose transcriptomics revealed overall downregulation of genes related to inflammatory processes after n-3 and upregulation after n-6, partly correlating with changes in circulatory markers. These data point to tissue-specific proinflammatory effects of high n-6 intake, but a net systemic anti-inflammatory effect as for n-3.
ω-3（n-3）（如二十碳五烯酸/二十二碳六烯酸[EPA/DHA]）和ω-6（n-6）（如亚油酸[LA]）脂肪酸对炎症的影响被认为相反，但结果并不一致，且缺乏n-3和n-6的直接比较。在一项双盲、随机、交叉研究中，对30至70岁腹部肥胖的女性（n = 16）和男性（n = 23）补充3-4克/天的EPA/DHA（鱼油）或15-20克/天的LA（红花油），为期7周，有9周的洗脱期。测量了细胞因子和趋化因子（多重检测）、急性期蛋白（基质辅助激光解吸电离飞行时间质谱）、内皮功能（血管反应指数）、血压、脂肪酸组成（红细胞膜/血清/脂肪组织，气相色谱-质谱/质谱）和脂肪基因表达（微阵列、定量聚合酶链反应）。虽然在收缩压的相对变化分数上发现治疗组之间存在显著差异（n-3与n-6：-1.81%对2.61%，P = 0.003），但在任何循环炎症标志物方面未发现n-3和n-6之间存在差异。然而，与基线相比，n-3组循环肿瘤坏死因子（TNF）降低（-24.9%，P < 0.001）、激活后正常T细胞表达和分泌的调节蛋白（-12.1%，P < 0.001）以及巨噬细胞炎性蛋白1-β降低（-12.5%，P = 0.014），n-6组TNF降低（-18.8%，P < 0.001）、激活后正常T细胞表达和分泌的调节蛋白降低（-7.37%，P = 0.027）、单核细胞趋化蛋白-1降低（-7.81%，P = 0.020）以及巨噬细胞炎性蛋白1-β降低（-14.2%，P = 0.010）。脂肪组织在EPA的重量百分比上显示出显著的治疗差异（n-3与n-6：50.2%∗对-1.38%，P < 0.001，∗：治疗组内显著变化分数）、DHA（16.0%∗对-3.67%，P < 0.001）和LA（-0.033对4.91%∗，P < 0.001）。脂肪转录组学显示，n-3后与炎症过程相关的基因总体下调，n-6后上调，部分与循环标志物的变化相关。这些数据表明高n-6摄入量具有组织特异性促炎作用，但n-3具有净全身抗炎作用。
