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ω-3 脂肪酸与胰岛素抵抗:聚焦于线粒体和内质网应激的调节。

Omega-3 Fatty Acids and Insulin Resistance: Focus on the Regulation of Mitochondria and Endoplasmic Reticulum Stress.

机构信息

Department of Chemistry and Biology, University of Salerno, Via Giovanni Paolo II, 132, Fisciano 84084, Italy.

Department of Biology, University of Naples Federico II, Complesso Universitario di Monte S.Angelo, Edificio 7, via Cintia 26, 80126 Napoli, Italy.

出版信息

Nutrients. 2018 Mar 14;10(3):350. doi: 10.3390/nu10030350.

DOI:10.3390/nu10030350
PMID:29538286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5872768/
Abstract

Mitochondrial dysfunction and endoplasmic reticulum (ER) stress have been suggested to play a key role in insulin resistance development. Reactive oxygen species (ROS) production and lipid accumulation due to mitochondrial dysfunction seemed to be important mechanisms leading to cellular insulin resistance. Moreover, mitochondria are functionally and structurally linked to ER, which undergoes stress in conditions of chronic overnutrition, activating the unfolded protein response, which in turn activates the principal inflammatory pathways that impair insulin action. Among the nutrients, dietary fats are believed to play key roles in insulin resistance onset. However, not all dietary fats exert the same effects on cellular energy metabolism. Dietary omega 3 polyunsaturated fatty acids (PUFA) have been suggested to counteract insulin resistance development by modulating mitochondrial bioenergetics and ER stress. In the current review, we summarized current knowledge on the role played by mitochondrial and ER stress in inflammation and insulin resistance onset, focusing on the modulation role of omega 3 PUFA on these stress pathways. Understanding the mechanisms by which omega 3 PUFA modulates cellular metabolism and insulin resistance in peripheral tissues may provide additional details on the potential impact of omega 3 PUFA on metabolic function and the management of insulin resistance in humans.

摘要

线粒体功能障碍和内质网(ER)应激被认为在胰岛素抵抗的发展中起关键作用。由于线粒体功能障碍导致的活性氧(ROS)产生和脂质积累似乎是导致细胞胰岛素抵抗的重要机制。此外,线粒体在功能和结构上与内质网相连,内质网在慢性营养过剩的情况下会受到应激,激活未折叠蛋白反应,进而激活主要的炎症途径,损害胰岛素的作用。在营养素中,膳食脂肪被认为在胰岛素抵抗的发生中起关键作用。然而,并非所有膳食脂肪对细胞能量代谢都有相同的影响。膳食ω-3 多不饱和脂肪酸(PUFA)被认为通过调节线粒体生物能学和内质网应激来对抗胰岛素抵抗的发展。在本综述中,我们总结了线粒体和内质网应激在炎症和胰岛素抵抗发生中的作用的最新知识,重点介绍了ω-3 PUFA 对这些应激途径的调节作用。了解 ω-3 PUFA 调节外周组织细胞代谢和胰岛素抵抗的机制,可以为 ω-3 PUFA 对代谢功能的潜在影响以及人类胰岛素抵抗的管理提供更多细节。

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