Ceddia Rolando B, Sweeney Gary
Department of Biology, York University, Toronto, M3J 1P3 Ontario, Canada.
J Physiol. 2004 Mar 1;555(Pt 2):409-21. doi: 10.1113/jphysiol.2003.056291. Epub 2004 Jan 14.
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 approximately 9.3- and approximately 5.1-fold, respectively, but the ATP content of the cells was not affected. Insulin significantly increased 2-deoxyglucose uptake ( approximately 1.9-fold), GLUT4 translocation ( approximately 1.8-fold), the incorporation of D-[U-(14)C]glucose into glycogen ( approximately 2.3-fold), lactate production ( approximately 1.5-fold) and (14)CO(2) production ( approximately 1.5-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 approximately 42% the basal rate of lactate production and increased by approximately 40% the basal rate of (14)CO(2) production. This is in agreement with the approximately 35% increase in citrate synthase activity and also with the approximately 2-fold increase in the phosphorylation of both alpha-1 and alpha-2 isoforms of AMPK after creatine supplementation. We conclude that 48 h 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.
最近的观察结果表明，补充肌酸可能对骨骼肌中的葡萄糖调节产生有益影响。然而，关于肌酸对葡萄糖摄取和代谢的直接影响的确定性研究尚缺。本研究的目的是调查补充肌酸对L6大鼠骨骼肌细胞中基础及胰岛素刺激的葡萄糖转运蛋白（GLUT4）转位、葡萄糖摄取、糖原含量、糖原合成、乳酸生成、葡萄糖氧化及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）、肌酸（0.5 mM）和肌酸 + 胰岛素。补充肌酸48小时后，L6成肌细胞中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含量未受影响。胰岛素显著增加了2-脱氧葡萄糖摄取（约1.9倍）、GLUT4转位（约1.8倍）、D-[U-(14)C]葡萄糖掺入糖原（约2.3倍）、乳酸生成（约1.5倍）和(14)CO(2)生成（约1.5倍）。肌酸既未改变细胞中的糖原和GLUT4含量，也未改变胰岛素刺激的2-DG摄取、GLUT4转位、糖原合成及葡萄糖氧化速率。然而，肌酸使基础乳酸生成速率显著降低了约42%，并使基础(14)CO(2)生成速率增加了约40%。这与补充肌酸后柠檬酸合酶活性增加约35%以及AMPK的α-1和α-2同工型磷酸化增加约2倍相一致。我们得出结论，补充肌酸48小时不会改变胰岛素刺激的葡萄糖摄取和葡萄糖代谢；然而，它会激活AMPK，使基础葡萄糖代谢转向氧化，并减少L6大鼠骨骼肌细胞中的乳酸生成。
