Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats.
Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats.
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维生素E和维生素C不会降低胰岛素敏感性，但会抑制运动肥胖大鼠的线粒体蛋白表达。
DOI：
10.1139/apnm-2014-0302
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Thyfault,JohnP
中科院分区：
文献类型：
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作者：
Picklo,MatthewJ;Thyfault,JohnP
关于补充抗氧化剂维生素E和维生素C是否会阻碍对运动的适应，存在争议。运动是治疗肥胖及其并发症的一线手段。虽然饮食诱导的肥胖改变线粒体功能并诱导胰岛素抵抗（IR），但没有数据表明补充维生素E和维生素C是否会改变先前存在的肥胖症患者对运动的反应。我们检验了以下假设：在维持高脂肪（45%脂肪能量（en））饮食的肥胖大鼠中，膳食补充维生素E（0.4 g α-生育酚乙酸酯/kg）和维生素C（0.5 g/kg）可阻断运动诱导的IR和线粒体含量改善。饮食诱导的肥胖，久坐大鼠有2倍更高的稳态模型评估胰岛素抵抗和更大的胰岛素曲线下面积以下的葡萄糖耐量试验比大鼠喂低脂（10%脂肪en）饮食。肥胖大鼠的运动（12周，每周5次，在机动轮中）使IR指数正常化，维生素E和维生素C没有改变这种效果。补充维生素E和维生素C与运动相比，以特定的方式在更大程度上（20%）提高脂肪和骨骼肌中的mtDNA含量。另一方面，维生素C和维生素E降低运动诱导的线粒体蛋白质含量增加的复合物I（40%）和烟酰胺核苷酸转氢酶（35%）在肌肉依赖性的方式。这些数据表明，维生素E和维生素C的补充肥胖啮齿动物不修改运动引起的胰岛素敏感性的改善，但线粒体生物合成和线粒体蛋白质表达的变化可能会被修改的抗氧化剂补充。
Controversy exists as to whether supplementation with the antioxidants vitamin E and vitamin C blocks adaptation to exercise. Exercise is a first-line means to treat obesity and its complications. While diet-induced obesity alters mitochondrial function and induces insulin resistance (IR), no data exist as to whether supplementation with vitamin E and vitamin C modify responses to exercise in pre-existing obesity. We tested the hypothesis that dietary supplementation with vitamin E (0.4 g α-tocopherol acetate/kg) and vitamin C (0.5 g/kg) blocks exercise-induced improvements on IR and mitochondrial content in obese rats maintained on a high-fat (45% fat energy (en)) diet. Diet-induced obese, sedentary rats had a 2-fold higher homeostasis model assessment of insulin resistance and larger insulin area under the curve following glucose tolerances test than rats fed a low-fat (10% fat en) diet. Exercising (12 weeks at 5 times per week in a motorized wheel) of obese rats normalized IR indices, an effect not modified by vitamin E and vitamin C. Vitamin E and vitamin C supplementation with exercise elevated mtDNA content in adipose and skeletal muscle to a greater extent (20%) than exercise alone in a depot-specific manner. On the other hand, vitamin C and vitamin E decreased exercise-induced increases in mitochondrial protein content for complex I (40%) and nicotinamide nucleotide transhydrogenase (35%) in a muscle-dependent manner. These data indicate that vitamin E and vitamin C supplementation in obese rodents does not modify exercise-induced improvements in insulin sensitivity but that changes in mitochondrial biogenesis and mitochondrial protein expression may be modified by antioxidant supplementation.