Abstract
Insulin stimulation of Glut 4 translocation requires the activation of phosphatidylinositol 3-kinase (PI 3-kinase) but the downstream pathway remains ill-defined. We demonstrated that the overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), a downstream effector of PI 3-kinase, stimulated Glut 4 translocation in adipocytes. This effect does not require the PH domain of PDK1, but expression of the pleckstrin homology domain-deleted PDK1 inhibits the effect of insulin, but not okadaic acid, on Glut 4 translocation. These results support a role of the PDK1 pathway in the transmission of insulin signal to Glut translocation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3-Phosphoinositide-Dependent Protein Kinases
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Adipocytes / drug effects*
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Adipocytes / metabolism
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Amino Acid Sequence
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Animals
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Antibodies, Monoclonal / immunology
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Biological Transport
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Cell Compartmentation
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Enzyme Induction
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Epitopes / immunology
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Glucose Transporter Type 4
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Insulin / pharmacology*
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Male
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Molecular Sequence Data
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Monosaccharide Transport Proteins / metabolism*
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Muscle Proteins*
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Okadaic Acid / pharmacology
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Protein Serine-Threonine Kinases / chemistry
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / physiology*
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Protein Structure, Tertiary
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Rats
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Rats, Wistar
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Sequence Deletion
Substances
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Antibodies, Monoclonal
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Epitopes
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Glucose Transporter Type 4
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Insulin
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Monosaccharide Transport Proteins
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Muscle Proteins
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Slc2a4 protein, rat
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Okadaic Acid
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3-Phosphoinositide-Dependent Protein Kinases
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Pdpk1 protein, rat
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Protein Serine-Threonine Kinases