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ω-3 衍生介质可抵抗肥胖引起的脂肪组织炎症。

Omega-3-derived mediators counteract obesity-induced adipose tissue inflammation.

机构信息

Department of Biochemistry and Molecular Genetics, Hospital Clínic, Centre Esther Koplowitz (CEK), IDIBAPS, Barcelona 08036, Spain; CIBERehd, Barcelona 08036, Spain.

出版信息

Prostaglandins Other Lipid Mediat. 2013 Dec;107:77-84. doi: 10.1016/j.prostaglandins.2013.05.003. Epub 2013 May 21.

DOI:10.1016/j.prostaglandins.2013.05.003
PMID:23707933
Abstract

Chronic low-grade inflammation in adipose tissue has been recognized as a key step in the development of obesity-associated complications. In obesity, the accumulation of infiltrating macrophages in adipose tissue and their phenotypic switch to M1-type dysregulate inflammatory adipokine production leading to obesity-linked insulin resistance. Resolvins are potent anti-inflammatory and pro-resolving mediators endogenously generated from omega-3 fatty acids that act as "stop-signals" of the inflammatory response promoting the resolution of inflammation. Recently, a deficit in the production of these endogenous anti-inflammatory signals has been demonstrated in obese adipose tissue. The restoration of their levels by either exogenous administration of these mediators or feeding omega-3-enriched diets, improves the inflammatory status of adipose tissue and ameliorates metabolic dysfunction. Here, we review the current knowledge on the role of these endogenous autacoids in the resolution of adipose tissue inflammation with special emphasis on their functional actions on macrophages.

摘要

脂肪组织中的慢性低度炎症已被认为是肥胖相关并发症发展的关键步骤。在肥胖中,浸润性巨噬细胞在脂肪组织中的积累及其向 M1 型的表型转变会导致炎症脂肪因子的产生失调,从而导致与肥胖相关的胰岛素抵抗。消退素是内源性产生的、来自ω-3 脂肪酸的强效抗炎和促解决介质,它们作为炎症反应的“停止信号”,促进炎症的解决。最近,已经证明在肥胖的脂肪组织中这些内源性抗炎信号的产生不足。通过外源性给予这些介质或食用富含 ω-3 的饮食来恢复它们的水平,可以改善脂肪组织的炎症状态并改善代谢功能障碍。在这里,我们综述了这些内源性自分泌物质在解决脂肪组织炎症中的作用的最新知识,特别强调了它们对巨噬细胞的功能作用。

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