Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle
Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle
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DOI：
10.1016/j.bbrc.2006.02.057
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发表时间：
2006-04-14
影响因子：
3.1
通讯作者：
Wojtaszewski, JFP
中科院分区：
文献类型：
--
作者：
Akerstrom, TCA;Birk, JB;Wojtaszewski, JFP
5'-AMP 激活蛋白激酶 (AMPK) 被认为是调节肌肉葡萄糖和脂肪代谢各个方面的“代谢主开关”。在离体大鼠骨骼肌中，葡萄糖会抑制 AMPK 的活性，而在人体肌肉中，糖原负荷会降低运动诱导的 AMPK 激活。我们假设运动期间口服葡萄糖的摄入会减弱肌肉 AMPK 的激活。九名男性受试者以最大负荷的 60% 进行了两次单腿膝关节伸肌运动。在两项试验中，受试者被随机分配饮用含葡萄糖饮料或安慰剂饮料。在运动前和运动后 2 小时对股外侧肌进行肌肉活检。血浆葡萄糖较高（6.0 +/- 0.2 vs. 4.9 +/- 0.1 mmol L-1，P < 0.001），而甘油（44.8 +/- 7.8 vs. 165.7 +/- 22.3 mu mol L-1）和游离脂肪酸（169.3 +/- 9.5 vs. 1161 +/- 144.9 mu mol）较高与安慰剂试验相比，葡萄糖试验期间 L-1) 浓度较低（均 P < 0.001）。葡萄糖试验期间计算的脂肪氧化较低（0.17 +/- 0.02 vs. 0.25 +/- 0.03 g min(-1)，P < 0.001）。与安慰剂试验相比，葡萄糖试验中 α 2-AMPK 的激活减弱（0.24 +/- 0.07 vs. 0.46 +/- 0.14 mu mol mg(-1) min(-1)，P = 0.03），而 α 1-AMPK 活性在试验之间没有差异，也不受运动的影响。 AMPK 和 AMPK 的下游靶标乙酰辅酶 A 羧化酶 β 因运动而被磷酸化，但两项试验之间没有显着差异。我们得出的结论是，口服葡萄糖摄入会减弱运动引起的 α2-AMPK 激活，从而进一步支持 AMPK 在骨骼肌中的燃料感应作用。 (c) 2006 Elsevier Inc. 保留所有权利。
5'-AMP-activated protein kinase (AMPK) has been suggested to be a 'metabolic master switch' regulating various aspects of muscle glucose and fat metabolism. In isolated rat skeletal muscle, glucose suppresses the activity of AMPK and in human muscle glycogen loading decreases exercise-induced AM PK activation. We hypothesized that oral glucose ingestion during exercise would attenuate muscle AMPK activation. Nine male subjects performed two bouts of one-legged knee-extensor exercise at 60% of maximal workload. The subjects were randomly assigned to either Consume a glucose containing drink or a placebo drink during the two trials. Muscle biopsies were taken from the vastus lateralis before and after 2 h of exercise. Plasma glucose was higher (6.0 +/- 0.2 vs. 4.9 +/- 0.1 mmol L-1, P < 0.001), whereas glycerol (44.8 +/- 7.8 vs. 165.7 +/- 22.3 mu mol L-1), and free fatty acid (169.3 +/- 9.5 vs. 1161 +/- 144.9 mu mol L-1) concentrations were lower during the glucose compared to the placebo trial (both P < 0.001). Calculated fat oxidation was lower during the glucose trial (0.17 +/- 0.02 vs. 0.25 +/- 0.03 g min(-1), P < 0.001). Activation of alpha 2-AMPK was attenuated in the glucose trial compared to the placebo trial (0.24 +/- 0.07 vs. 0.46 +/- 0.14 mu mol mg(-1) min(-1), P = 0.03), whereas the alpha 1-AMPK activity was not different between trials or affected by exercise. AMPK and the downstream target of AMPK, acetyl-CoA carboxylase-beta, were phosphorylated as a response to exercise, but neither was significantly different between the two trials. We conclude that oral glucose ingestion attenuates the exercise-induced activation of alpha 2-AMPK, bringing further support for a fuel-sensing role of AMPK in skeletal muscle. (c) 2006 Elsevier Inc. All rights reserved.