Creatine supplementation increases glucose oxidation and AMPK phosphorylation and reduces lactate production in L6 rat skeletal muscle cells
Creatine supplementation increases glucose oxidation and AMPK phosphorylation and reduces lactate production in L6 rat skeletal muscle cells
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DOI：
10.1113/jphysiol.2003.056291
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发表时间：
2004-03-01
影响因子：
5.5
通讯作者：
Sweeney, G
中科院分区：
文献类型：
--
作者：
Ceddia, RB;Sweeney, G
最近的观察表明，肌酸补充可能对骨骼肌的葡萄糖调节有有益的影响。然而，肌酸对葡萄糖摄取和代谢的直接影响的结论性研究还缺乏。本研究的目的是研究补充肌酸对L 6大鼠骨骼肌细胞基础和胰岛素刺激的葡萄糖转运蛋白（GLUT 4）转位、葡萄糖摄取、糖原含量、糖原合成、乳酸产生、葡萄糖氧化和AMP激活的蛋白激酶（AMPK）磷酸化的影响。研究了四个治疗组：对照组、胰岛素（100 nm）组、肌酸（0.5 nm）组和肌酸+胰岛素组。补充肌酸48小时后，L 6成肌细胞的肌酸和磷酸肌酸含量分别增加了约9.3倍和约5.1倍，但细胞的ATP含量没有受到影响。胰岛素显著增加2-脱氧葡萄糖摄取（接近1.9倍）、GLUT 4易位（接近1.8倍）、D- [U-C-14]葡萄糖掺入糖原（接近2.3倍）、乳酸产生（接近1.5倍）和（CO2）-C-14产生（接近1.5倍）。肌酸既不改变糖原和GLUT 4含量的细胞，也不胰岛素刺激率的2-DG摄取，GLUT 4易位，糖原合成和葡萄糖氧化。然而，肌酸显著降低了乳酸产生的基础速率约42%，并增加了（CO2）-C-14产生的基础速率约40%。这与补充肌酸后柠檬酸合酶活性增加35%和AMPK α-1和α-2亚型磷酸化增加2倍的结果一致。我们的结论是，48它的肌酸补充不改变胰岛素刺激的葡萄糖摄取和葡萄糖代谢，但是，它激活AMPK，转向氧化的基础葡萄糖代谢，并减少L 6大鼠骨骼肌细胞中的乳酸产生。
Recent observations have suggested that creatine supplementation might have a beneficial effect on glucoregulation in skeletal muscle. However, conclusive studies on the direct effects of creatine on glucose uptake and metabolism are lacking. The objective of this study was to investigate the effects of creatine supplementation on basal and insulin-stimulated glucose transporter (GLUT4) translocation, glucose uptake, glycogen content, glycogen synthesis, lactate production, glucose oxidation and AMP-activated protein kinase (AMPK) phosphorylation in L6 rat skeletal muscle cells. Four treatment groups were studied: control, insulin (100 nm), creatine (0.5 mm) and creatine + insulin. After 48 h of creatine supplementation the creatine and phosphocreatine contents of L6 myoblasts increased by similar to9.3- and similar to5.1-fold, respectively, but the ATP content of the cells was not affected. Insulin significantly increased 2-deoxyglucose uptake (similar to 1.9-fold), GLUT4 translocation (similar to 1.8-fold), the incorporation of D- [U-C-14] glucose into glycogen (similar to2.3-fold), lactate production (similar to1.5-fold) and (CO2)-C-14 production (similar to1.5-fold). Creatine neither altered the glycogen and GLUT4 contents of the cells nor the insulin-stimulated rates of 2-DG uptake, GLUT4 translocation, glycogen synthesis and glucose oxidation. However, creatine significantly reduced by similar to42% the basal rate of lactate production and increased by similar to40% the basal rate of (CO2)-C-14 production. This is in agreement with the similar to35% increase in citrate synthase activity and also with the similar to2-fold increase in the phosphorylation of both alpha-1 and alpha-2 isoforms of AMPK after creatine supplementation. We conclude that 48 It of creatine supplementation does not alter insulin-stimulated glucose uptake and glucose metabolism; however, it activates AMPK, shifts basal glucose metabolism towards oxidation and reduces lactate production in L6 rat skeletal muscle cells.