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共轭亚油酸(CLA)通过过氧化物酶体增殖物激活受体δ介导的机制提高小鼠的耐力。

Conjugated linoleic acid (CLA) promotes endurance capacity via peroxisome proliferator-activated receptor δ-mediated mechanism in mice.

作者信息

Kim Yoo, Kim Daeyoung, Park Yeonhwa

机构信息

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

Department of Mathematics and Statistics, University of Massachusetts, Amherst, MA 01003, USA.

出版信息

J Nutr Biochem. 2016 Dec;38:125-133. doi: 10.1016/j.jnutbio.2016.08.005. Epub 2016 Sep 7.

Abstract

Previously, it was reported that conjugated linoleic acid (CLA) with exercise training potentially improved endurance capacity via the peroxisome proliferator-activated receptor δ (PPARδ)-mediated mechanism in mice. This study determined the role of exercise and/or CLA in endurance capacity and PPARδ-associated regulators. Male 129Sv/J mice were fed either control (soybean oil) or CLA (0.5%) containing diets for 4 weeks and were further divided into sedentary or training regimes. CLA supplementation significantly reduced body weight and fat mass independent of exercise during the experimental period. Endurance capacity was significantly improved by CLA supplementation, while no effect of exercise was observed. Similarly, CLA treatment significantly increased expressions of sirtuin 1 and PPARγ coactivator-1α, up-stream regulators of PPARδ, in both sedentary and trained animals. With respect to downstream markers of PPARδ, CLA up-regulated the key biomarker needed to stimulate mitochondrial biogenesis, nuclear respiratory factor 1. Moreover, CLA supplementation significantly induced overall genes associated with muscle fibers, such as type I (slow-twitch) and type II (fast twitch). Taken together, it suggests that CLA improves endurance capacity independent of mild-intensity exercise via PPARδ-mediated mechanism.

摘要

此前有报道称,共轭亚油酸(CLA)与运动训练相结合,可能通过过氧化物酶体增殖物激活受体δ(PPARδ)介导的机制提高小鼠的耐力。本研究确定了运动和/或CLA在耐力以及与PPARδ相关的调节因子中的作用。将雄性129Sv/J小鼠分为两组,分别喂食对照(大豆油)或含0.5%CLA的饮食,为期4周,然后进一步分为久坐组或训练组。在实验期间,补充CLA显著降低了体重和脂肪量,且与运动无关。补充CLA显著提高了耐力,而未观察到运动的影响。同样,CLA处理显著增加了久坐和训练小鼠中PPARδ的上游调节因子——沉默调节蛋白1和PPARγ共激活因子-1α的表达。关于PPARδ的下游标志物,CLA上调了刺激线粒体生物发生所需的关键生物标志物——核呼吸因子1。此外,补充CLA显著诱导了与肌肉纤维相关的整体基因,如I型(慢肌纤维)和II型(快肌纤维)。综上所述,这表明CLA通过PPARδ介导的机制提高耐力,与轻度运动无关。

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