UCP-3 expression in skeletal muscle: effects of exercise, hypoxia, and AMP-activated protein kinase.
UCP-3 expression in skeletal muscle: effects of exercise, hypoxia, and AMP-activated protein kinase.
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DOI：
10.1152/ajpendo.2000.279.3.e622
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发表时间：
2000-09
期刊：
影响因子：
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通讯作者：
Mina I. Zhou;B. Lin;S. Coughlin;G. Vallega;P. Pilch
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文献类型：
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作者：
Mina I. Zhou;B. Lin;S. Coughlin;G. Vallega;P. Pilch
解偶联蛋白 3 (UCP-3) 是线粒体转运蛋白超家族的成员，主要在骨骼肌中表达，在禁食和运动等引起的燃料消耗条件下，它可能在改变代谢功能方面发挥作用。在这里，我们表明，大鼠在跑步机上快速跑步（30 分钟）会诱导骨骼肌 UCP-3 mRNA 表达（200 分钟后增加七倍），缺氧和以相对快速和大量的方式游泳也是如此。线粒体转运蛋白、肉毒碱棕榈酰转移酶 1 和三羧酸盐载体的表达在这些条件下不受影响。缺氧和运动介导的 UCP-3 mRNA 诱导导致大鼠 UCP-3 蛋白相应增加四到六倍。我们用 5'-氨基-4-咪唑甲酰胺核糖核苷 (AICAR) 治疗趾长伸肌 (EDL)，AICAR 是一种激活 AMP 激活蛋白激酶 (AMPK) 的化合物，AMP 激活蛋白激酶是一种已知在运动和缺氧过程中受到刺激的酶。与未处理的肌肉相比，将大鼠 EDL 肌肉与 2 mM AICAR 体外孵育 30 分钟，导致 UCP-3 mRNA 增加三倍，UCP-3 蛋白增加 1.5 倍。这些数据与 AMPK 的激活（可能是燃料耗尽的结果）快速调节 UCP-3 基因表达的观点一致。
Uncoupling protein 3 (UCP-3), a member of the mitochondrial transporter superfamily, is expressed primarily in skeletal muscle where it may play a role in altering metabolic function under conditions of fuel depletion caused, for example, by fasting and exercise. Here, we show that treadmill running by rats rapidly (30 min) induces skeletal muscle UCP-3 mRNA expression (sevenfold after 200 min), as do hypoxia and swimming in a comparably rapid and substantial fashion. The expression of the mitochondrial transporters, carnitine palmitoyltransferase 1 and the tricarboxylate carrier, is unaffected under these conditions. Hypoxia and exercise-mediated induction of UCP-3 mRNA result in a corresponding four- to sixfold increase in rat UCP-3 protein. We treated extensor digitorum longus (EDL) muscle with 5'-amino-4-imidazolecarboxamide ribonucleoside (AICAR), a compound that activates AMP-activated protein kinase (AMPK), an enzyme known to be stimulated during exercise and hypoxia. Incubation of rat EDL muscle in vitro for 30 min with 2 mM AICAR causes a threefold increase in UCP-3 mRNA and a 1.5-fold increase of UCP-3 protein compared with untreated muscle. These data are consistent with the notion that activation of AMPK, presumably as a result of fuel depletion, rapidly regulates UCP-3 gene expression.