Abstract
In skeletal muscle, glucose transport is stimulated by insulin, contractions and hypoxia. In this study, we used the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin to examine whether (i) PI 3-kinase activity is necessary for stimulation of glucose transport by insulin in muscle, and (ii) PI 3-kinase mediates a step in the pathway by which contractions/hypoxia stimulate glucose transport. Wortmannin completely blocked insulin- and insulin-like growth factor-1-stimulated glucose transport in muscle. In contrast, wortmannin had no effect on the stimulation of glucose transport by contractions or hypoxia, providing evidence that PI 3-kinase activity is not involved in the activation of glucose transport by these stimuli.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Androstadienes / pharmacology*
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Animals
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Biological Transport / drug effects
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Cell Hypoxia
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Culture Techniques
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Glucose / metabolism*
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Insulin / pharmacology
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Insulin-Like Growth Factor I / pharmacology
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Male
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Muscle Contraction / physiology
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Muscle, Skeletal / drug effects
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Muscle, Skeletal / enzymology*
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Phosphatidylinositol 3-Kinases
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Phosphotransferases (Alcohol Group Acceptor) / antagonists & inhibitors
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Phosphotransferases (Alcohol Group Acceptor) / physiology*
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Rats
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Rats, Wistar
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Wortmannin
Substances
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Androstadienes
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Insulin
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Insulin-Like Growth Factor I
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Phosphatidylinositol 3-Kinases
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Phosphotransferases (Alcohol Group Acceptor)
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Glucose
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Wortmannin