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饮食中的长链而非中链甘油三酯会损害大鼠的运动表现并使心脏线粒体解偶联。

Dietary long-chain, but not medium-chain, triglycerides impair exercise performance and uncouple cardiac mitochondria in rats.

机构信息

Department of Physiology, Anatomy & Genetics, University of Oxford, Parks Rd, Oxford, OX1 3PT, UK.

出版信息

Nutr Metab (Lond). 2011 Aug 1;8:55. doi: 10.1186/1743-7075-8-55.

DOI:10.1186/1743-7075-8-55
PMID:21806803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3168416/
Abstract

Short-term consumption of a high-fat diet impairs exercise capacity in both rats and humans, and increases expression of the mitochondrial uncoupling protein, UCP3, in rodent cardiac and skeletal muscle via activation of the transcription factor, peroxisome proliferator-activated receptor α (PPARα). Unlike long-chain fatty acids however, medium-chain fatty acids do not activate PPARα and do not increase muscle UCP3 expression. We therefore investigated exercise performance and cardiac mitochondrial function in rats fed a chow diet (7.5% kcal from fat), a long-chain triglyceride (LCT) rich diet (46% kcal from LCTs) or a medium-chain triglyceride (MCT) rich diet (46% kcal from MCTs). Rats fed the LCT-rich diet for 15 days ran 55% less far than they did at baseline, whereas rats fed the chow or MCT-rich diets neither improved nor worsened in their exercise capacities. Moreover, consumption of an LCT-rich diet increased cardiac UCP3 expression by 35% and decreased oxidative phosphorylation efficiency, whereas consumption of the MCT-rich diet altered neither UCP3 expression nor oxidative phosphorylation efficiency. Our results suggest that the negative effects of short-term high-fat feeding on exercise performance are predominantly mediated by long-chain rather than medium-chain fatty acids, possibly via PPARα-dependent upregulation of UCP3.

摘要

短期摄入高脂肪饮食会降低大鼠和人类的运动能力,通过激活转录因子过氧化物酶体增殖物激活受体α(PPARα),增加啮齿动物心脏和骨骼肌中线粒体解偶联蛋白 UCP3 的表达。然而,与长链脂肪酸不同,中链脂肪酸不会激活 PPARα,也不会增加肌肉 UCP3 的表达。因此,我们研究了给予普通饮食(7.5%的热量来自脂肪)、富含长链甘油三酯(LCT)的饮食(46%的热量来自 LCT)或富含中链甘油三酯(MCT)的饮食(46%的热量来自 MCT)的大鼠的运动表现和心脏线粒体功能。给予富含 LCT 的饮食 15 天的大鼠比基线时少跑 55%,而给予普通饮食或富含 MCT 的饮食的大鼠的运动能力既没有提高也没有恶化。此外,富含 LCT 的饮食会使心脏 UCP3 的表达增加 35%,并降低氧化磷酸化效率,而富含 MCT 的饮食既不会改变 UCP3 的表达,也不会改变氧化磷酸化效率。我们的结果表明,短期高脂肪喂养对运动能力的负面影响主要是由长链脂肪酸而不是中链脂肪酸介导的,可能通过 PPARα 依赖性上调 UCP3。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/1f34d130afe3/1743-7075-8-55-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/b4ff337730c6/1743-7075-8-55-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/44176cb0fc47/1743-7075-8-55-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/b2d59bba9c3a/1743-7075-8-55-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/1f34d130afe3/1743-7075-8-55-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/b4ff337730c6/1743-7075-8-55-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/44176cb0fc47/1743-7075-8-55-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/b2d59bba9c3a/1743-7075-8-55-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedb/3168416/1f34d130afe3/1743-7075-8-55-4.jpg

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