Mu J, Brozinick J T, Valladares O, Bucan M, Birnbaum M J
Howard Hughes Medical Institute, The Cox Institute, The Department of Medicine, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.
Mol Cell. 2001 May;7(5):1085-94. doi: 10.1016/s1097-2765(01)00251-9.
Eukaryotic cells possess systems for sensing nutritional stress and inducing compensatory mechanisms that minimize the consumption of ATP while utilizing alternative energy sources. Such stress can also be imposed by increased energy needs, such as in skeletal muscle of exercising animals. In these studies, we consider the role of the metabolic sensor, AMP-activated protein kinase (AMPK), in the regulation of glucose transport in skeletal muscle. Expression in mouse muscle of a dominant inhibitory mutant of AMPK completely blocked the ability of hypoxia or AICAR to activate hexose uptake, while only partially reducing contraction-stimulated hexose uptake. These data indicate that AMPK transmits a portion of the signal by which muscle contraction increases glucose uptake, but other AMPK-independent pathways also contribute to the response.
真核细胞拥有感知营养应激并诱导补偿机制的系统，这些机制在利用替代能源时将ATP的消耗降至最低。这种应激也可能由能量需求增加引起，比如在运动动物的骨骼肌中。在这些研究中，我们探讨了代谢传感器——AMP激活的蛋白激酶（AMPK）在骨骼肌葡萄糖转运调节中的作用。在小鼠肌肉中表达AMPK的显性抑制突变体完全阻断了缺氧或AICAR激活己糖摄取的能力，而仅部分降低收缩刺激的己糖摄取。这些数据表明，AMPK传递了肌肉收缩增加葡萄糖摄取的部分信号，但其他不依赖AMPK的途径也参与了这一反应。
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