A mitochondrial-targeted ubiquinone modulates muscle lipid profile and improves mitochondrial respiration in obesogenic diet-fed rats
A mitochondrial-targeted ubiquinone modulates muscle lipid profile and improves mitochondrial respiration in obesogenic diet-fed rats
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DOI：
10.1017/s0007114515005528
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发表时间：
2016-04-14
影响因子：
3.6
通讯作者：
Feillet-Coudray, Christine
中科院分区：
文献类型：
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作者：
Coudray, Charles;Fouret, Gilles;Feillet-Coudray, Christine
包括腹部肥胖、血脂异常和胰岛素抵抗在内的代谢综合征各组成部分的流行率在发达国家和发展中国家都在增加。人们普遍认为，这些特征的发展是在线粒体功能受损之前或伴随着线粒体功能受损。本研究旨在分析一种靶向脂溶性泛醌（MitoQ）对致肥胖饮食喂养大鼠肌肉脂质分布调节和线粒体功能的影响。为此，将24只年轻雄性Sprague-Dawley大鼠分为三组，并喂食以下饮食之一：（1）对照，（2）高脂肪（HF）和（3）HF+MitoQ。8周后，测量骨骼肌中的线粒体功能标志物和脂质代谢/概况改变。HF饮食在诱导代谢综合征的主要特征方面是有效的，即肥胖、肝脏肿大和葡萄糖耐受不良。MitoQ摄入可防止大鼠体重增加，减弱脂肪组织和肝脏重量的增加，并部分逆转葡萄糖耐受不良。在肌肉水平上，HF饮食诱导与肌肉磷脂类和总肌肉脂质的脂肪酸组成的重要修改相关的中度TAG积累。这些脂质修饰伴随着线粒体呼吸的减少。MitoQ摄入纠正了脂质改变并恢复了线粒体呼吸。这些结果表明，MitoQ通过其对肌肉脂质代谢和线粒体活性的影响，保护肥胖饮食喂养的大鼠免受代谢综合征的某些特征的影响。这些发现表明，MitoQ是未来代谢综合征预防人体试验的一个有希望的候选者。
The prevalence of the metabolic syndrome components including abdominal obesity, dyslipidaemia and insulin resistance is increasing in both developed and developing countries. It is generally accepted that the development of these features is preceded by, or accompanied with, impaired mitochondrial function. The present study was designed to analyse the effects of a mitochondrial-targeted lipophilic ubiquinone (MitoQ) on muscle lipid profile modulation and mitochondrial function in obesogenic diet-fed rats. For this purpose, twenty-four young male Sprague-Dawley rats were divided into three groups and fed one of the following diets: (1) control, (2) high fat (HF) and (3) HF+MitoQ. After 8 weeks, mitochondrial function markers and lipid metabolism/profile modifications in skeletal muscle were measured. The HF diet was effective at inducing the major features of the metabolic syndrome - namely, obesity, hepatic enlargement and glucose intolerance. MitoQ intake prevented the increase in rat body weight, attenuated the increase in adipose tissue and liver weights and partially reversed glucose intolerance. At the muscle level, the HF diet induced moderate TAG accumulation associated with important modifications in the muscle phospholipid classes and in the fatty acid composition of total muscle lipid. These lipid modifications were accompanied with decrease in mitochondrial respiration. MitoQ intake corrected the lipid alterations and restored mitochondrial respiration. These results indicate that MitoQ protected obesogenic diet-fed rats from some features of the metabolic syndrome through its effects on muscle lipid metabolism and mitochondrial activity. These findings suggest that MitoQ is a promising candidate for future human trials in the metabolic syndrome prevention.