Immuno-Resolving Ability of Resolvins, Protectins, and Maresins Derived from Omega-3 Fatty Acids in Metabolic Syndrome.,Molecular Nutrition & Food Research

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Immuno-Resolving Ability of Resolvins, Protectins, and Maresins Derived from Omega-3 Fatty Acids in Metabolic Syndrome.
Molecular Nutrition & Food Research ( IF 4.5 ) Pub Date : 2019-12-15 , DOI: 10.1002/mnfr.201900824
Youngjoo Kwon ₁

Affiliation

Omega‐3 fatty acid consumption has been suggested to be beneficial for the prevention of type 2 diabetes mellitus (T2DM). Its effects have been attributed to anti‐inflammatory activity, with the inhibition of arachidonic acid metabolism playing a central role. However, a more recent view is that omega‐3 fatty acids play an active role as the precursors of potent, specialized pro‐resolving mediators (SPMs), such as resolvins, protectins, and maresins. Docosahexaenoic acid (DHA)‐ and eicosapentaenoic‐acid‐derived SPMs are identified in the adipose tissue but the levels of certain SPMs (e.g., protectin D1) are markedly reduced with obesity, suggesting adipose SPM deficiency, potentially resulting in unresolved inflammation. Supplementation of the biosynthetic intermediates of SPM (e.g., 17‐hydroxy‐DHA) or omega‐3 fatty acids increases the level of adipose SPMs, reduces adipose inflammation (decrease in macrophage accumulation and change to less inflammatory macrophages), and enhances insulin sensitivity. The findings from studies using rodent obesity models must be translated to humans. It will be important to further elucidate the underlying mechanisms by which obesity reduces the levels of and the sensitivity to SPM in adipose tissues. This will enable the development of nutrition therapy to enhance the effects of omega‐3 fatty acids in the prevention and/or treatment of T2DM.

中文翻译：

代谢综合征中衍生自Omega-3脂肪酸的Resolvins，Proteins和Maresins的免疫分辨能力。

有人建议食用Omega-3脂肪酸有助于预防2型糖尿病（T2DM）。它的作用归因于抗炎活性，其中花生四烯酸代谢的抑制起着核心作用。但是，最近的观点是，ω-3脂肪酸作为强力，专门的亲分解介体（SPM）的前体发挥着积极的作用，例如间苯二酚，保护素和马瑞森。在脂肪组织中发现了二十二碳六烯酸（DHA）和二十碳五烯酸衍生的SPM，但是某些SPM（例如保护素D1）的水平随着肥胖而显着降低，表明脂肪SPM不足，可能导致炎症未解决。补充SPM的生物合成中间体（例如，17-羟基-DHA）或omega-3脂肪酸可增加脂肪SPM的水平，减少脂肪发炎（减少巨噬细胞的积累，并减少发炎的巨噬细胞），并增强胰岛素敏感性。使用啮齿类肥胖症模型进行的研究发现必须转化为人类。重要的是，进一步阐明肥胖降低脂肪组织中SPM的水平和对SPM的敏感性的潜在机制。这将有助于营养治疗的发展，从而增强omega-3脂肪酸在预防和/或治疗T2DM中的作用。重要的是，进一步阐明肥胖降低脂肪组织中SPM的水平和对SPM的敏感性的潜在机制。这将有助于营养治疗的发展，从而增强omega-3脂肪酸在预防和/或治疗T2DM中的作用。重要的是，进一步阐明肥胖降低脂肪组织中SPM的水平和对SPM的敏感性的潜在机制。这将有助于营养治疗的发展，从而增强omega-3脂肪酸在预防和/或治疗T2DM中的作用。

更新日期：2019-12-15

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