Mølvig J, Pociot F, Worsaae H, Wogensen L D, Baek L, Christensen P, Mandrup-Poulsen T, Andersen K, Madsen P, Dyerberg J
Steno Memorial Hospital, Hagedorn Research Laboratory, Gentofte, Denmark.
Scand J Immunol. 1991 Oct;34(4):399-410. doi: 10.1111/j.1365-3083.1991.tb01563.x.
The effects of dietary supplementation with omega-3-polyunsaturated fatty acids (omega-3-PUFA) on the proliferative response of PBMC and on the secretion of monokines and arachidonic acid metabolites from PBMC and monocytes (Mo) from healthy subjects and patients with recent-onset insulin-dependent diabetes mellitus (IDDM) were examined. Three groups of eight to nine healthy individuals were randomized to either 2.0 g/day or 4.0 g/day of omega-3-PUFA devoid of vitamins A and D, or an isocaloric amount of placebo. Furthermore, eight patients with recent-onset IDDM received 4.0 g/day of omega-3-PUFA. IL-1 beta production and TNF-alpha secretion was determined before and after 7 weeks of treatment, and 10 weeks after withdrawal of treatment. Significant increases in platelet and PBMC membrane eicosapentaenoic acid was found in omega-3-PUFA-treated individuals. omega-3-PUFA treatment significantly reduced the content of IL-1 beta in lysates of PBMC, but did not affect PBMC or Mo secretion of IL-1 beta, TNF-alpha or prostaglandin E2 (PGE2) or PBMC leukotriene B4 (LTB4) secretion in healthy subjects or in IDDM patients. A significant inhibition of the PHA-stimulated, but not the spontaneous or PPD-stimulated, proliferative response of PBMC was observed in healthy and diabetic subjects treated with omega-3-PUFA. No correlation was found between PHA-stimulated PBMC proliferation and PBMC secretion of TNF-alpha and IL-1 beta. There were no significant differences in the spontaneous or the PPD- or PHA-stimulated proliferative responses of PBMC between diabetic and healthy individuals at entry. We conclude that although dietary supplementation with 4.0 g/day of omega-3-PUFA inhibits the proliferation of PBMC and reduces IL-1 beta immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects.
研究了补充ω-3多不饱和脂肪酸（ω-3-PUFA）饮食对健康受试者和近期发病的胰岛素依赖型糖尿病（IDDM）患者外周血单核细胞（PBMC）增殖反应以及PBMC和单核细胞（Mo）中单核因子和花生四烯酸代谢产物分泌的影响。将三组8至9名健康个体随机分为两组，分别每日补充2.0克或4.0克不含维生素A和D的ω-3-PUFA，或等量的安慰剂。此外，8名近期发病的IDDM患者每日接受4.0克ω-3-PUFA。在治疗7周前后以及停药10周后测定白细胞介素-1β（IL-1β）的产生和肿瘤坏死因子-α（TNF-α）的分泌。在接受ω-3-PUFA治疗的个体中，发现血小板和PBMC膜中的二十碳五烯酸显著增加。ω-3-PUFA治疗显著降低了PBMC裂解物中IL-1β的含量，但不影响健康受试者或IDDM患者PBMC或Mo分泌IL-1β、TNF-α或前列腺素E2（PGE2），也不影响PBMC白三烯B4（LTB4）的分泌。在用ω-3-PUFA治疗的健康和糖尿病受试者中，观察到PBMC对PHA刺激的增殖反应受到显著抑制，但对自发或PPD刺激的增殖反应无影响。未发现PHA刺激的PBMC增殖与PBMC分泌TNF-α和IL-1β之间存在相关性。在入组时，糖尿病个体和健康个体之间PBMC的自发、PPD或PHA刺激的增殖反应无显著差异。我们得出结论，尽管每日补充4.0克ω-3-PUFA饮食可抑制PBMC增殖并降低PBMC和Mo中IL-1β的免疫反应性，但它不会改变健康或IDDM受试者中单核因子、PGE2或LTB4的分泌。
