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首页> 外文期刊>Journal of Cellular Physiology >Enhanced lipid-but not carbohydrate-supported mitochondrial respiration in skeletal muscle of PGC-1α overexpressing mice
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Enhanced lipid-but not carbohydrate-supported mitochondrial respiration in skeletal muscle of PGC-1α overexpressing mice

机译：增强lipid-but不是carbohydrate-supported在骨骼肌线粒体呼吸PGC-1αoverexpressing老鼠

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摘要

Skeletal muscle mitochondrial dysfunction has been linked to several disease states as well as the process of aging. A possible factor involved is the peroxisome proliferator-activated receptor (PPAR) γ co-activator 1α (PGC-1α), a major player in the regulation of skeletal muscle mitochondrial metabolism. However, it is currently unknown whether PGC-1α, besides stimulating mitochondrial proliferation, also affects the functional capacity per mitochondrion. Therefore, we here tested whether PGC-1α overexpression, besides increasing mitochondrial content, also leads to intrinsic mitochondrial adaptations. Skeletal muscle mitochondria from 10 male, muscle-specific PGC-1α overexpressing mice (PGC-1αTg) and 8 wild-type (WT) mice were isolated. Equal mitochondrial quantities were then analyzed for their oxidative capacity by high-resolution respirometry, fuelled by a carbohydrate-derived (pyruvate) and a lipid (palmitoyl-CoA plus carnitine) substrate. Additionally, mitochondria were tested for reactive oxygen species (superoxide) production and fatty acid (FA)-induced uncoupling. PGC-1αTg mitochondria were characterized by an improved intrinsic mitochondrial fat oxidative capacity as evidenced by pronounced increase in ADP-stimulated respiration (P<0.001) and maximal uncoupled respiration (P<0.001) upon palmitoyl-CoA plus carnitine. Interestingly, intrinsic mitochondrial capacity on a carbohydrate-derived substrate tended to be reduced. Furthermore, the sensitivity to FA-induced uncoupling was diminished in PGC-1αTg mitochondria (P=0.02) and this was accompanied by a blunted reduction in mitochondrial ROS production upon FAs in PGC-1αTg versus WT mitochondria (P=0.04). Uncoupling protein 3 (UCP3) levels were markedly reduced in PGC-1αTg mitochondria (P<0.001). Taken together, in addition to stimulating mitochondrial proliferation in skeletal muscle, we show here that overexpression of PGC-1α leads to intrinsic mitochondrial adaptations that seem restricted to fat metabolism.
机译：骨骼肌线粒体功能障碍与一些疾病以及衰老的过程。的过氧物酶体proliferator-activated受体(PPARγco-activator 1α(PGC-1α),一个重要的球员在骨骼肌的规定线粒体代谢。目前未知是否PGC-1α,除了刺激线粒体增生影响了每个功能的能力线粒体。PGC-1α超表达,除了增加线粒体的内容,也会导致内在线粒体的适应性。线粒体从10男,阳性PGC-1αoverexpressing老鼠(PGC-1αTg)和8个野生型(WT)老鼠孤立。为他们的氧化量进行分析能力通过高分辨率的呼吸运动计量法,加剧了由carbohydrate-derived(丙酮酸)和脂质(palmitoyl-CoA +肉碱)衬底。此外,线粒体进行了测试活性氧(过氧化物)生产和脂肪酸(FA)全身的解偶联。线粒体是一种改进的特征内在线粒体脂肪氧化的能力显示明显的增加ADP-stimulated呼吸作用(P < 0.001)和最大非耦合呼吸作用(P < 0.001)palmitoyl-CoA +肉碱。内在的线粒体上的能力carbohydrate-derived衬底倾向减少了。FA-induced解偶联减少在PGC-1αTg线粒体(P = 0.02),这是伴随着钝化减少线粒体ROS生产在FAs PGC-1αTg和WT线粒体(P = 0.04)。(UCP3)水平显著降低PGC-1αTg线粒体(P < 0.001)。除了刺激线粒体在骨骼肌扩散,我们显示在这里过度的PGC-1α导致内在线粒体适应性似乎限制脂肪代谢。

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