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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Augmenting muscle diacylglycerol and triacylglycerol content by blocking fatty acid oxidation does not impede insulin sensitivity
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Augmenting muscle diacylglycerol and triacylglycerol content by blocking fatty acid oxidation does not impede insulin sensitivity

机译：通过阻断脂肪酸氧化来增加肌肉中二酰甘油和三酰甘油的含量不会影响胰岛素敏感性

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摘要

Alow fat oxidative capacity has been linked to muscle diacylglycerol (DAG) accumulation and insulin resistance. Alternatively, a low fat oxidation rate may stimulate glucose oxidation, thereby enhancing glucose disposal. Here, we investigated whether an ethyl-2-[6-(4-chlorophenoxy)hexyl]-oxirane-2-carboxylate (etomoxir)-induced in-hibition of fat oxidation leads to muscle fat storage and insulin resistance. An intervention in healthy male subjects was combined with studies in human primary myotubes. Furthermore, muscle DAG and triacylglycerol (TAG), mitochondrial function, and insulin signaling were examined in etomoxir-treated C57bl6 mice. In humans, etomoxir administration increased glucose oxidation at the expense of fat oxidation. This effect was accompanied by an increased abundance of GLUT4 at the sarcolemma and a lowering of plasma glucose levels, indicative of improved glucose homeostasis. In mice, etomoxir injections resulted in accumulation of muscle TAG and DAG, yet improved insulin-stimulated GLUT4 translocation. Also in human myotubes, insulin signaling was improved by etomoxir, in the presence of increased intramyocellular lipid accumulation. These insulin-sensitizing effects in mice and human myotubes were accompanied by increased phosphorylation of AMP-activated protein kinase (AMPK). Our results show that a reduction in fat oxidation leading to accumulation of muscle DAG does not necessarily lead to insulin resistance, as the reduction in fat oxidation may activate AMPK.
机译：脂肪氧化能力低与肌肉二酰基甘油（DAG）积累和胰岛素抵抗有关。可选地，低的脂肪氧化速率可以刺激葡萄糖氧化，从而增强葡萄糖的处置。在这里，我们调查了2- [6-（4-（4-氯苯氧基）己基]-环氧乙烷-2-羧酸乙酯（依托莫司）诱导的脂肪氧化抑制是否导致肌肉脂肪储存和胰岛素抵抗。健康男性受试者的干预措施与人类原代肌管的研究相结合。此外，在依托莫司治疗的C57bl6小鼠中检查了肌肉DAG和三酰基甘油（TAG），线粒体功能和胰岛素信号传导。在人类中，依托莫司的给药增加了葡萄糖的氧化，但以脂肪氧化为代价。这种作用伴随着肌膜处GLUT4丰度的增加和血浆葡萄糖水平的降低，这表明改善了葡萄糖稳态。在小鼠中，依托莫昔注射导致肌肉TAG和DAG积累，但改善了胰岛素刺激的GLUT4易位。同样在人肌管中，在肌细胞内脂质蓄积增加的情况下，依托莫司改善了胰岛素信号传导。这些在小鼠和人肌管中的胰岛素增敏作用伴随着AMP活化蛋白激酶（AMPK）磷酸化的增加。我们的结果表明，导致肌肉DAG积累的脂肪氧化减少不一定导致胰岛素抵抗，因为脂肪氧化减少可能会激活AMPK。

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