Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in patients with metabolic syndrome.
Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in patients with metabolic syndrome.
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DOI：
10.2337/dc12-1161
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发表时间：
2013-05
期刊：
影响因子：
16.2
通讯作者：
Tsutsui H
中科院分区：
文献类型：
--
作者：
Yokota T;Kinugawa S;Yamato M;Hirabayashi K;Suga T;Takada S;Harada K;Morita N;Oyama-Manabe N;Kikuchi Y;Okita K;Tsutsui H
全身性氧化应激与胰岛素抵抗和肥胖有关。我们测试了代谢综合征(METS)患者全身氧化应激与有氧能力降低和骨骼肌功能障碍有关的假说。对14例男性METS患者和13例年龄、性别和活动相匹配的健康受试者进行了自行车功率计递增负荷运动试验。用血清硫代巴比妥酸反应物质(TBARS)评价系统脂质过氧化反应，用血清总硫醇和超氧化物歧化酶(SOD)活性评价系统抗氧化防御能力。为了评估骨骼肌的能量代谢，我们分别使用31P和1质子磁共振波谱测量了小腿屈足运动时小腿肌肉中的高能磷酸盐和休息时腿部肌肉中的肌内脂质(IMCL)。与健康对照组比较，METS患者血清总硫醇和超氧化物歧化酶活性显著降低(分别为290.8±51.2vs 398.7±105.2μμ/L和22.2±8.4vs 31.5±8.5U/L，P<；0.05)。METS患者的最大氧耗量和无氧阈值分别降低了25%和31%，并与血清−呈负相关(r=−0.49和r=0.50)。此外，运动中肌肉磷酸肌酸的损失是甲亢组的1.4倍(P<；0.05)，肌间黏附分子含量是甲亢组的2.9倍(P<；0.01)，提示骨骼肌能量代谢受损，这些指标与血清总胆红素呈正相关(分别为r=0.45和r=0.63)。代谢综合征患者全身氧化应激与有氧能力降低和骨骼肌能量代谢受损有关。
Systemic oxidative stress is associated with insulin resistance and obesity. We tested the hypothesis that systemic oxidative stress is linked to lower aerobic capacity and skeletal muscle dysfunction in metabolic syndrome (MetS). The incremental exercise testing with cycle ergometer was performed in 14 male patients with MetS and 13 age-, sex-, and activity-matched healthy subjects. Systemic lipid peroxidation was assessed by serum thiobarbituric acid reactive substances (TBARS), and systemic antioxidant defense capacity was assessed by serum total thiols and enzymatic activity of superoxide dismutase (SOD). To assess skeletal muscle energy metabolism, we measured high-energy phosphates in the calf muscle during plantar flexion exercise and intramyocellular lipid (IMCL) in the resting leg muscle, using 31P- and 1proton-magnetic resonance spectroscopy, respectively. Serum TBARS were elevated (12.4 ± 7.1 vs. 3.7 ± 1.1 μmol/L; P < 0.01), and serum total thiols and SOD activity were decreased (290.8 ± 51.2 vs. 398.7 ± 105.2 μmol/L, P < 0.01; and 22.2 ± 8.4 vs. 31.5 ± 8.5 units/L, P < 0.05, respectively) in patients with MetS compared with healthy subjects. Peak VO2 and anaerobic threshold normalized to body weight were significantly lower in MetS patients by 25 and 31%, respectively, and inversely correlated with serum TBARS (r = −0.49 and r = −0.50, respectively). Moreover, muscle phosphocreatine loss during exercise was 1.4-fold greater in patients with MetS (P < 0.05), and IMCL content was 2.9-fold higher in patients with MetS (P < 0.01), indicating impaired skeletal muscle energy metabolism, and these indices positively correlated with serum TBARS (r = 0.45 and r = 0.63, respectively). Systemic oxidative stress was associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in patients with MetS.
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