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首页> 外文期刊>The Journal of Nutritional Biochemistry >Long-term follow-up of muscle lipid accumulation, mitochondrial activity and oxidative stress and their relationship with impaired glucose homeostasis in high fat high fructose diet-fed rats
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Long-term follow-up of muscle lipid accumulation, mitochondrial activity and oxidative stress and their relationship with impaired glucose homeostasis in high fat high fructose diet-fed rats

机译：长期随访肌肉脂质积累，线粒体活性和氧化应激及其与高脂肪高果糖饮食饮食饲料大鼠的葡萄糖稳态的关系

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Metabolic syndrome components, including obesity, dyslipidemia and impaired glucose homeostasis, become a major public health issue. Muscles play a predominant role in insulin-mediated glucose uptake, and high fat diets may negatively affect muscle function and homeostasis. This work aimed to study the time-course of muscle lipid accumulation, oxidative stress and mitochondrial dysfunction and their association to impaired glucose homeostasis in rats fed an obesogenic diet. Male Wistar rats were fed with a standard or a high fat/high fructose (HFHFr) diet and sacrificed on 4, 8, 12, 16, 20 weeks. Rats fed the HFHFr diet developed mild overweight, increased liver and adipose tissue weights and glucose intolerance. The impaired glucose homeostasis increased gradually with the HFHFr diet to become significant on the 12th and 16th weeks of diet. In parallel, the muscle lipid composition showed an increase in the saturated fatty acids and the monounsaturated fatty acids with a marked decrease in the polyunsaturated fatty acids. The HFHFr diet also increased muscle contents of both diacylglycerols and Ceramides. Surprisingly, HFHFr diet did not induce major muscle mitochondrial dysfunction or oxidative stress. These results indicate that muscle lipid alterations, as well as impaired glucose homeostasis occur as early as the 8th week of HFHFr diet, increase to reach a plateau around the 12th-16th weeks of diet, and then attenuate towards the end of study. At these diet treatment durations, muscle mitochondrial activity and oxidative stress remained unchanged and do not seem to have a major role in the observed impaired glucose homeostasis. (C) 2018 Elsevier Inc. All rights reserved.
机译：代谢综合征组分，包括肥胖，血脂血症和葡萄糖稳态受损，成为一个主要的公共卫生问题。肌肉在胰岛素介导的葡萄糖摄取中发挥主要作用，高脂肪饮食可能对肌肉功能和稳态产生负面影响。这项工作旨在研究肌肉脂质积累，氧化应激和线粒体功能障碍及其在喂养obesogensic饮食的大鼠中葡萄糖稳态的关联的时间才能研究。雄性Wistar大鼠用标准或高脂肪/高果糖（HFHFR）饮食，并在4,8,12,16,20周内牺牲。喂养HFHFR饮食的大鼠显得轻度超重，增加肝脏和脂肪组织重量和葡萄糖不耐受。受损的葡萄糖稳态随着HFHFR饮食逐渐增加，在饮食的第12和第16周内变得显着。平行，肌肉脂质组合物显示饱和脂肪酸的增加和单不饱和脂肪酸的增加，该脂肪酸在多不饱和脂肪酸中显着降低。 HFHFR饮食也增加了二酰基甘油和神经酰胺的肌肉含量。令人惊讶的是，HFHFR饮食没有诱导主要肌肉线粒体功能障碍或氧化应激。这些结果表明，肌肉脂质改变，以及葡萄糖稳定性的血糖稳定性受损，早在HFHFR饮食的第8周发生，增加到饮食12-16周左右的高原，然后在研究结束时衰减。在这些饮食治疗持续时间内，肌肉线粒体活性和氧化应激保持不变，似乎在观察到的葡萄糖稳态中似乎没有重要作用。 （c）2018年Elsevier Inc.保留所有权利。

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