Undecanesulfonate does not allosterically activate H+ uniport mediated by uncoupling protein-1 in brown adipose tissue mitochondria.
Undecanesulfonate does not allosterically activate H+ uniport mediated by uncoupling protein-1 in brown adipose tissue mitochondria.
复制标题
十一烷磺酸盐不会变构激活棕色脂肪组织线粒体中由解偶联蛋白 1 介导的 H uniport。
DOI：
10.1016/j.biocel.2006.05.011
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Jabůrek,Martin
中科院分区：
文献类型：
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作者：
Jezek,Petr;Spacek,Tomás;Garlid,Keith;Jabůrek,Martin
十一烷磺酸盐通过解偶联蛋白-1转运。它不能诱导重组解偶联蛋白-1的H+单通道支持脂肪酸循环假说。Rial等人[Rial，E.，Aguirregoitia，E.，Jimenez-Jimenez，J.，& Ledesma，A.（2004年）。烷基磺酸盐激活解偶联蛋白UCP 1：对运输机制的影响。Biochimica et Bioprophilica Acta，1608，122-130]已经通过观察由于十一烷磺酸盐引起的棕色脂肪组织线粒体的解偶联来挑战脂肪酸循环，解偶联被解释为解偶联蛋白-1的变构活化。我们估计十一烷磺酸盐的影响消除内源性脂肪酸的肉毒碱循环在存在或不存在牛血清白蛋白。我们表明，十一烷磺酸盐的效果是部分由于脂肪酸从白蛋白释放时，十一烷磺酸盐释放结合脂肪酸和部分代表一个非特异性的解偶联蛋白独立的呼吸加速，因为它也在大鼠心脏线粒体缺乏解偶联蛋白-1和膜电位不降低后，除了十一烷磺酸盐没有白蛋白。当测定净脂肪酸诱导的解偶联时，添加十一烷磺酸盐甚至轻微抑制解偶联呼吸。我们得出结论，十一烷磺酸盐不变构激活解偶联蛋白-1，脂肪酸循环不能排除其非特异性作用的基础上。
Undecanesulfonate is transported by uncoupling protein-1. Its inability to induce H+uniport with reconstituted uncoupling protein-1 supports fatty acid cycling hypothesis. Rial et al. [Rial, E., Aguirregoitia, E., Jimenez-Jimenez, J., & Ledesma, A. (2004). Alkylsulfonates activate the uncoupling protein UCP1: Implications for the transport mechanism. Biochimica et Biophysica Acta, 1608, 122–130], have challenged the fatty acid cycling by observing uncoupling of brown adipose tissue mitochondria due to undecanesulfonate, interpreted as allosteric activation of uncoupling protein-1. We have estimated undecanesulfonate effects after elimination of endogenous fatty acids by carnitine cycle in the presence or absence of bovine serum albumin. We show that the undecanesulfonate effect is partly due to fatty acid release from albumin when undecanesulfonate releases bound fatty acid and partly represents a non-specific uncoupling protein-independent acceleration of respiration, since it proceeds also in rat heart mitochondria lacking uncoupling protein-1 and membrane potential is not decreased upon addition of undecanesulfonate without albumin. When the net fatty acid-induced uncoupling was assayed, the addition of undecanesulfonate even slightly inhibited the uncoupled respiration. We conclude that undecanesulfonate does not allosterically activate uncoupling protein-1 and that fatty acid cycling cannot be excluded on a basis of its non-specific effects.