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Creatine supplementation increases glucose oxidation and AMPK phosphorylation and reduces lactate production in L6 rat skeletal muscle cells
Author(s) -
Ceddia Rolando B.,
Sweeney Gary
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.056291
Subject(s) - medicine , glut4 , endocrinology , glycogen , creatine , phosphocreatine , glycogen synthase , glucose transporter , glucose uptake , skeletal muscle , insulin , ampk , basal (medicine) , creatine kinase , biology , chemistry , metabolism , phosphorylation , biochemistry , protein kinase a , energy metabolism
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 n m ), creatine (0.5 m m ) and creatine + insulin. After 48 h of creatine supplementation the creatine and phosphocreatine contents of L6 myoblasts increased by ∼9.3‐ and ∼5.1‐fold, respectively, but the ATP content of the cells was not affected. Insulin significantly increased 2‐deoxyglucose uptake (∼1.9‐fold), GLUT4 translocation (∼1.8‐fold), the incorporation of D‐[U‐ 14 C]glucose into glycogen (∼2.3‐fold), lactate production (∼1.5‐fold) and 14 CO 2 production (∼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 ∼42% the basal rate of lactate production and increased by ∼40% the basal rate of 14 CO 2 production. This is in agreement with the ∼35% increase in citrate synthase activity and also with the ∼2‐fold increase in the phosphorylation of both α‐1 and α‐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.