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首页> 美国卫生研究院文献>The Journal of Physiology >Fatty acids stimulate AMP-activated protein kinase and enhance fatty acid oxidation in L6 myotubes
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Fatty acids stimulate AMP-activated protein kinase and enhance fatty acid oxidation in L6 myotubes

机译：脂肪酸刺激AMP激活的蛋白激酶并增强L6肌管中的脂肪酸氧化

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摘要

We investigated the role of fatty acid availability on AMPK signalling and fatty acid oxidation in skeletal muscle. Incubating L6 skeletal muscle myotubes with palmitate (a saturated fatty acid) or linoleate (a polyunsaturated fatty acid) increased AMPK activity by 56 and 38%, respectively, compared with untreated cells. Consistent with these changes, AMPK Thr172 and acetyl-CoA carboxylase β Ser218 phosphorylation were increased in fatty acid treated cells. Pre-incubating cells with palmitate or linoleate increased subsequent fatty acid oxidation by 86 and 92%, respectively. The enhanced AMPK signalling occurred in the absence of detectable changes in free AMP and glycogen content. The activity of the upstream kinase LKB1 was decreased by fatty acid treatment indicating that AMPK activation was not a consequence of LKB1 activation. Instead, fatty acids enhanced LKB1 phosphorylation of AMPK. Fatty acids did not alter LKB1 activity when either synthetic peptide or AMPK α(1–312) catalytic fragment was used as substrate indicating that the βγ subunits were required for the fatty acid activation. Infection of cells with a dominant-negative AMPK adenovirus reduced basal fatty acid oxidation and inhibited the stimulatory effects of fatty acid pretreatment on fatty acid oxidation. These results indicate that increasing fatty acid availability increases AMPK activity independent of changes in the cellular energy charge and support the view that fatty acids may modulate AMPK allosterically, making it a better substrate for LKB1.
机译：我们调查了脂肪酸可用性对骨骼肌中AMPK信号和脂肪酸氧化的作用。与未经处理的细胞相比，将L6骨骼肌肌管与棕榈酸酯（一种饱和脂肪酸）或亚油酸酯（一种多不饱和脂肪酸）一起培养，可使AMPK活性分别提高56％和38％。与这些变化一致，在脂肪酸处理的细胞中AMPK Thr 172 和乙酰辅酶A羧化酶βSer 218 的磷酸化增加。用棕榈酸酯或亚油酸酯预孵育细胞后，随后的脂肪酸氧化分别增加了86％和92％。增强的AMPK信号传导发生在游离AMP和糖原含量没有可检测的变化的情况下。脂肪酸处理降低了上游激酶LKB1的活性，表明AMPK激活不是LKB1激活的结果。相反，脂肪酸增强了AMPK的LKB1磷酸化。当使用合成肽或AMPKα（1-312）催化片段作为底物时，脂肪酸不会改变LKB1活性，表明βγ亚基是脂肪酸活化所必需的。用显性阴性AMPK腺病毒感染细胞可减少基础脂肪酸氧化并抑制脂肪酸预处理对脂肪酸氧化的刺激作用。这些结果表明，增加的脂肪酸利用率增加了AMPK的活性，而与细胞能量电荷的变化无关，并支持脂肪酸可能会变构地调节AMPK的观点，从而使其成为LKB1的较好底物。

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