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An involvement of the mitochondrial fatty acid transporters in the development of myocellular insulin resistance

机译:线粒体脂肪酸转运蛋白参与肌细胞胰岛素抵抗的发展

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Long-chain fatty acids (LCFAs) are an important source of energy for working skeletal muscles. The predominant mechanism of LCFA influx into skeletal muscle involves sarcolemmal proteins, namely fatty-acid transporters. Recent studies imply strong correlations between increased plasmalemmal expression of FA transporters and the development of insulin resistance in skeletal muscles. However, it seems that a major feature of myocyte insulin resistance is the imbalance in lipid transport into the cells and the capacity of mitochondria for LCFA oxidation. Excess deposition of myocelluar fatty acids leads to the accumulation of triacylglycerols, diacyloglycerols, and ceramides. Most likely, the accumulation of intramuscular lipid fractions is responsible for disturbances in the insulin signaling pathway and the subsequent development of skeletal muscle insulin resistance.
机译:长链脂肪酸(LCFA)是工作骨骼肌的重要能量来源。 LCFA流入骨骼肌的主要机制涉及肌膜蛋白,即脂肪酸转运蛋白。最近的研究表明,FA转运蛋白的血浆表达增加与骨骼肌胰岛素抵抗的发展之间存在很强的相关性。然而,似乎心肌细胞胰岛素抵抗的一个主要特征是脂质向细胞内转运的不平衡以及线粒体的LCFA氧化能力。肌细胞脂肪酸的过量沉积导致三酰基甘油,二酰基甘油和神经酰胺的积累。肌内脂质部分的积累最有可能导致胰岛素信号传导途径的紊乱以及骨骼肌胰岛素抵抗的后续发展。

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