Chanseaume Emilie, Giraudet Christophe, Gryson Céline, Walrand Stéphane, Rousset Paulette, Boirie Yves, Morio Béatrice
Lipid and Energy Metabolism Research Unit, Human Nutrition Laboratory, Institut National de la Recherche Agronomique, Unité Mixte de Recherche 1019, Clermont-Ferrand cedex 1, France.
Obesity (Silver Spring). 2007 Apr;15(4):853-9. doi: 10.1038/oby.2007.582.
Obesity and insulin resistance are associated with muscle mitochondrial dysfunction, which might be related to impairment of mitochondrial protein synthesis. This study aimed at investigating mixed and mitochondrial protein synthesis in skeletal muscle in response to dietary manipulations.
High-sucrose (SU) and high-fat, high-sucrose (F) diets were provided for 6 weeks to Wistar rats at standard (N) and high (H) energy intakes and compared with controls. Fractional synthesis rates of mixed (FSRPT) and mitochondrial (FSRm) proteins within the oxidative (soleus) and glycolytic (tibialis) muscles were measured using stable isotope flooding dose technique using L-[13C]-valine. Carbonyl content, citrate synthase, and cytochrome c oxidase activities were assayed spectrophotometrically on isolated mitochondria.
In the soleus, FSRPT was increased by 40% in the NSU and NF groups and by 65% in the HSU and HF groups (p<0.001 vs. control). FSRm was increased with high-fat diets (NF, +16%; HF, +32%; p<0.01). In the tibialis, FSR(PT) was enhanced in all experimental groups (+31% to 37%, p<0.05 vs. control). FSRm was augmented in the NSU, NF, and HF groups (+28% to 32%, p<0.01). Cytochrome c oxidase activity was significantly decreased in all experimental groups in the soleus (p<0.001).
Muscle mixed and mitochondrial protein FSR are enhanced after short-term dietary intervention known to induce insulin resistance and obesity. Adaptations are muscle type specific and may not explain alterations in mitochondrial oxidative capacity but might contribute to maintain mitochondrial functioning.
肥胖和胰岛素抵抗与肌肉线粒体功能障碍有关,这可能与线粒体蛋白质合成受损有关。本研究旨在调查骨骼肌中混合蛋白和线粒体蛋白合成对饮食干预的反应。
以标准(N)和高(H)能量摄入量,给Wistar大鼠提供高蔗糖(SU)和高脂肪、高蔗糖(F)饮食6周,并与对照组进行比较。使用L-[13C]-缬氨酸的稳定同位素灌流剂量技术测量氧化型(比目鱼肌)和糖酵解型(胫骨前肌)肌肉中混合蛋白(FSRPT)和线粒体蛋白(FSRm)的分数合成率。通过分光光度法测定分离线粒体中的羰基含量、柠檬酸合酶和细胞色素c氧化酶活性。
在比目鱼肌中,NSU和NF组的FSRPT增加了40%,HSU和HF组增加了65%(与对照组相比,p<0.001)。高脂肪饮食使FSRm增加(NF组增加16%;HF组增加32%;p<0.01)。在胫骨前肌中,所有实验组的FSR(PT)均增强(增加31%至37%,与对照组相比,p<0.05)。NSU、NF和HF组的FSRm增加(增加28%至32%,p<0.01)。所有实验组比目鱼肌中的细胞色素c氧化酶活性均显著降低(p<0.001)。
在已知会诱导胰岛素抵抗和肥胖的短期饮食干预后,肌肉混合蛋白和线粒体蛋白的FSR增强。适应性变化具有肌肉类型特异性,可能无法解释线粒体氧化能力的改变,但可能有助于维持线粒体功能。