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首页> 外文期刊>Molecular and Cellular Biology >Leptin Stimulates Fatty Acid Oxidation and Peroxisome Proliferator-Activated Receptor α Gene Expression in Mouse C2C12 Myoblasts by Changing the Subcellular Localization of the α2 Form of AMP-Activated Protein Kinase
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Leptin Stimulates Fatty Acid Oxidation and Peroxisome Proliferator-Activated Receptor α Gene Expression in Mouse C2C12 Myoblasts by Changing the Subcellular Localization of the α2 Form of AMP-Activated Protein Kinase

机译：瘦素刺激小鼠氧化C2C12成肌细胞中的脂肪酸氧化和过氧化物酶体增殖物激活的受体α基因表达，通过改变AMP激活的蛋白激酶的α2形式的亚细胞定位。

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Leptin stimulates fatty acid oxidation in skeletal muscle through the activation of AMP-activated protein kinase (AMPK) and the induction of gene expression, such as that for peroxisome proliferator-activated receptor α (PPARα). We now show that leptin stimulates fatty acid oxidation and PPARα gene expression in the C2C12 muscle cell line through the activation of AMPK containing the α2 subunit (α2AMPK) and through changes in the subcellular localization of this enzyme. Activated α2AMPK containing the β1 subunit was shown to be retained in the cytoplasm, where it phosphorylated acetyl coenzyme A carboxylase and thereby stimulated fatty acid oxidation. In contrast, α2AMPK containing the β2 subunit transiently increased fatty acid oxidation but underwent rapid translocation to the nucleus, where it induced PPARα gene transcription. A nuclear localization signal and Thr172 phosphorylation of α2 were found to be essential for nuclear translocation of α2AMPK, whereas the myristoylation of β1 anchors α2AMPK in the cytoplasm. The prevention of α2AMPK activation and the change in its subcellular localization inhibited the metabolic effects of leptin. Our data thus suggest that the activation of and changes in the subcellular localization of α2AMPK are required for leptin-induced stimulation of fatty acid oxidation and PPARα gene expression in muscle cells.
机译：瘦蛋白通过激活AMP激活的蛋白激酶（AMPK）和诱导基因表达来刺激骨骼肌中的脂肪酸氧化，例如过氧化物酶体增殖物激活的受体α（PPARα）。现在我们显示，瘦素通过激活包含α2亚基（α2AMPK）的AMPK并通过改变该酶的亚细胞定位来刺激C2C12肌肉细胞系中的脂肪酸氧化和PPARα基因表达。含有β1亚基的活化的α2AMPK被证明保留在细胞质中，在细胞质中它使乙酰辅酶A羧化酶磷酸化，从而刺激了脂肪酸的氧化。相反，含有β2亚基的α2AMPK瞬时增加了脂肪酸的氧化，但迅速转移到细胞核，从而诱导了PPARα基因的转录。发现α2的核定位信号和Thr 172 磷酸化对于α2AMPK的核易位至关重要，而β1的肉豆蔻酸化则将α2AMPK锚定在细胞质中。阻止α2AMPK激活及其亚细胞定位的变化抑制了瘦素的代谢作用。因此，我们的数据表明，α2AMPK的激活和亚细胞定位的改变对于瘦素诱导的肌肉细胞中脂肪酸氧化和PPARα基因表达的刺激是必需的。

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