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首页> 外文期刊>Cell metabolism >Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle.
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Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle.

机译：AMPK和SIRT1在代谢适应骨骼肌禁食和运动中的相互依赖性。

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摘要

During fasting and after exercise, skeletal muscle efficiently switches from carbohydrate to lipid as the main energy source to preserve glycogen stores and blood glucose levels for glucose-dependent tissues. Skeletal muscle cells sense this limitation in glucose availability and transform this information into transcriptional and metabolic adaptations. Here we demonstrate that AMPK acts as the prime initial sensor that translates this information into SIRT1-dependent deacetylation of the transcriptional regulators PGC-1alpha and FOXO1, culminating in the transcriptional modulation of mitochondrial and lipid utilization genes. Deficient AMPK activity compromises SIRT1-dependent responses to exercise and fasting, resulting in impaired PGC-1alpha deacetylation and blunted induction of mitochondrial gene expression. Thus, we conclude that AMPK acts as the primordial trigger for fasting- and exercise-induced adaptations in skeletal muscle and that activation of SIRT1 and its downstream signaling pathways are improperly triggered in AMPK-deficient states.
机译：在禁食和运动后，骨骼肌有效地从碳水化合物转变为脂质，将其作为主要能量来源，以保留糖原存储和葡萄糖依赖性组织的血糖水平。骨骼肌细胞感觉到葡萄糖利用率的限制，并将该信息转化为转录和代谢适应。在这里，我们证明AMPK充当主要的初始传感器，它将这些信息转换为转录调节因子PGC-1alpha和FOXO1的SIRT1依赖性脱乙酰基，最终导致线粒体和脂质利用基因的转录调控。不足的AMPK活性损害了对运动和禁食的SIRT1依赖性反应，导致受损的PGC-1alpha脱乙酰基作用和线粒体基因表达的钝化诱导。因此，我们得出结论，AMPK充当骨骼肌禁食和运动诱发的适应的原始触发器，并且在AMPK缺乏状态下SIRT1及其下游信号通路的激活被不正确地触发。

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