在骨骼肌葡萄糖autoregulates吸收:活化蛋白激酶的参与。
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Itani想知道如果萨哈AK, Kurowski TG,棺材人力资源,Tornheim K, Ruderman NB
在骨骼肌葡萄糖autoregulates吸收:活化蛋白激酶的参与。
糖尿病。2003年7月,52 (7):1635 - 40。
- PubMed ID
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12829626 (在PubMed]
- 文摘
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预曝光的低浓度葡萄糖上调葡萄糖运输到骨骼肌,而暴露在高浓度的葡萄糖有相反的效果。这个独立于胰岛素,自动调整的过程和机制,其运作是不完全理解。激活energy-sensing酶活化蛋白激酶(AMPK)被证明能增加胰岛素依赖葡萄糖运输到骨骼肌在运动和缺氧等刺激。在目前的研究中,我们调查了AMPK是否也可以调节葡萄糖自动调整。AMPK的alpha2对碘氧基苯甲醚的活动和2-deoxyglucose吸收评估孵化鼠趾长伸肌肌腱牵向前肌肉在媒体包含0,预培养4 h后3、6日或25更易与葡萄糖/ l。主要研究结果如下。首先,AMPK活性最高的肌肉孵化与不添加葡萄糖,它减少葡萄糖的浓度增加。符合这些发现,丙二酰辅酶a的浓度增加,乙酰辅酶a羧化酶磷酸化丝氨酸79下降为中葡萄糖浓度提高。第二,减少AMPK活性在高葡萄糖浓度与减少葡萄糖运输密切相关(2-deoxyglucose吸收),测量在随后的6点20分钟孵化更易与l葡萄糖(r (2) = 0.93, P < 0.001)。第三,减少AMPK活性在高葡萄糖浓度与变化无关whole-tissue磷酸肌酸的浓度或腺嘌呤核苷酸; however, it did correlate with increases in the rate of glycolysis, as estimated by lactate release. The results suggest that glucose autoregulates its own transport into skeletal muscle by a mechanism involving AMPK. They also suggest that this autoregulatory mechanism is not paralleled by changes in whole-tissue concentrations of creatine phosphate ATP, or AMP, but they leave open the possibility that alterations in a cytosolic pool of these compounds play a regulatory role.