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N-3 多不饱和脂肪酸通过几种炎症介质调节脂质代谢:预防肥胖的机制和意义。

N-3 polyunsaturated fatty acids regulate lipid metabolism through several inflammation mediators: mechanisms and implications for obesity prevention.

机构信息

Department of Animal Science, National Taiwan University, Taipei, Taiwan.

出版信息

J Nutr Biochem. 2010 May;21(5):357-63. doi: 10.1016/j.jnutbio.2009.09.010. Epub 2010 Feb 9.

Abstract

Obesity is a growing problem that threatens the health and welfare of a large proportion of the human population. The n-3 polyunsaturated fatty acids (PUFA) are dietary factors that have potential to facilitate reduction in body fat deposition and improve obesity-induced metabolic syndromes. The n-3 PUFA up-regulate several inflammation molecules including serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in hepatocytes and adipocytes. Actions of these inflammation mediators resemble those of n-3 PUFA in the modulation of many lipid metabolism-related genes. For instance, they both suppress expressions of perilipin, sterol regulatory element binding protein-1 (SREBP-1) and lipoprotein lipase (LPL) to induce lipolysis and reduce lipogenesis. This review will connect these direct or indirect regulating pathways between n-3 PUFA, inflammation mediators, lipid metabolism-related genes and body fat reduction. A thorough knowledge of these regulatory mechanisms will lead us to better utilization of n-3 PUFA to reduce lipid deposition in the liver and other tissues, therefore presenting an opportunity for developing new strategies to treat obesity.

摘要

肥胖是一个日益严重的问题,威胁着很大一部分人口的健康和福利。n-3 多不饱和脂肪酸(PUFA)是一种饮食因素,具有促进减少体脂肪沉积和改善肥胖引起的代谢综合征的潜力。n-3 PUFA 可上调肝细胞和脂肪细胞中的几种炎症分子,包括血清淀粉样蛋白 A(SAA)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)。这些炎症介质的作用类似于 n-3 PUFA 对许多与脂质代谢相关的基因的调节。例如,它们都抑制 perilipin、固醇调节元件结合蛋白-1(SREBP-1)和脂蛋白脂肪酶(LPL)的表达,以诱导脂肪分解和减少脂肪生成。本综述将连接 n-3 PUFA、炎症介质、与脂质代谢相关的基因与体脂减少之间的这些直接或间接调节途径。深入了解这些调节机制将使我们能够更好地利用 n-3 PUFA 来减少肝脏和其他组织中的脂质沉积,从而为开发治疗肥胖症的新策略提供机会。

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