Abstract
Vanadate stimulates adipocyte 2-deoxyglucose transport and GLUT-4 translocation to the membrane through an insulin receptor-independent but wortmannin-inhibitable pathway. Vanadate stimulates PI 3-kinase in anti-IRS-1 immunoprecipitates and the binding between IRS-1 and the p85alpha subunit of PI 3-kinase. In insulin-resistant adipocytes from old rats vanadate fully stimulates IRS-1-associated PI 3-kinase, but partially activates glucose uptake. We conclude that: (a) vanadate stimulates 2-deoxyglucose uptake using a pathway that converges with that of insulin at the level of PI 3-kinase; and (b) adipocytes from old rats are defective in the insulin pathway at steps located both upstream and downstream of PI 3-kinase.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipocytes / drug effects
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Adipocytes / metabolism*
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Animals
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Cells, Cultured
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Deoxyglucose / pharmacokinetics
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Enzyme Activation
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Glucose Transporter Type 4
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Insulin / pharmacology
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Insulin Receptor Substrate Proteins
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Male
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Monosaccharide Transport Proteins / metabolism
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Muscle Proteins*
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Phosphatidylinositol 3-Kinases / metabolism*
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Phosphoproteins / metabolism*
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Quercetin / pharmacology
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Rats
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Rats, Wistar
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Vanadates / pharmacology*
Substances
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Glucose Transporter Type 4
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Insulin
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Insulin Receptor Substrate Proteins
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Irs1 protein, rat
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Monosaccharide Transport Proteins
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Muscle Proteins
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Phosphoproteins
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Slc2a4 protein, rat
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Vanadates
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Deoxyglucose
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Quercetin
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Phosphatidylinositol 3-Kinases