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骨骼肌线粒体对肥胖、运动和多不饱和脂肪酸的适应性

Adaptations of Skeletal Muscle Mitochondria to Obesity, Exercise, and Polyunsaturated Fatty Acids.

作者信息

Chen Phoebe B, Yang Jason S, Park Yeonhwa

机构信息

Department of Food Science, University of Massachusetts, Amherst, 102 Holdsworth Way, Amherst, MA, 01003, USA.

出版信息

Lipids. 2018 Mar;53(3):271-278. doi: 10.1002/lipd.12037. Epub 2018 Apr 16.

DOI:10.1002/lipd.12037
PMID:29663395
Abstract

Mitochondria intricately modulate their energy production through the control of mitochondrial adaptation (mitochondrial biogenesis, fusion, and/or fission) to meet energy demands. Nutrient overload may result in dysregulated mitochondrial biogenesis, morphology toward mitochondrial fragmentation, and oxidative stress in the skeletal muscle. In addition, physical activity and diet components influence mitochondrial function. Exercise may stimulate mitochondrial biogenesis and promote mitochondrial fusion/fission in the skeletal muscle. Moreover, some dietary fatty acids, such as n-3 polyunsaturated fatty acids and conjugated linoleic acid, have been identified to positively regulate mitochondrial adaptation in the skeletal muscle. This review discusses the association of mitochondrial impairments and obesity, and presents an overview of various mechanisms of which exercise training and mitochondrial nutrients promote mitochondrial function in the skeletal muscle.

摘要

线粒体通过控制线粒体适应性(线粒体生物发生、融合和/或裂变)来精细调节其能量产生,以满足能量需求。营养过剩可能导致线粒体生物发生失调、线粒体形态趋向碎片化以及骨骼肌氧化应激。此外,身体活动和饮食成分会影响线粒体功能。运动可能刺激骨骼肌中的线粒体生物发生并促进线粒体融合/裂变。此外,一些膳食脂肪酸,如n-3多不饱和脂肪酸和共轭亚油酸,已被证实可正向调节骨骼肌中的线粒体适应性。本综述讨论了线粒体损伤与肥胖的关联,并概述了运动训练和线粒体营养素促进骨骼肌线粒体功能的各种机制。

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