Abstract
Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. These effects might contribute to the antidiabetic effect of troglitazone in obese diabetic animals.
MeSH terms
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3T3 Cells / chemistry
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3T3 Cells / cytology*
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3T3 Cells / drug effects
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Adipocytes / chemistry
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Adipocytes / cytology*
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Adipocytes / drug effects
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Animals
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Blood Glucose / analysis
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Cell Differentiation / drug effects
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Chromans / pharmacology*
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Cytokines / pharmacology*
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Drug Interactions
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Gene Expression Regulation
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Glucose / pharmacokinetics
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Glucose Transporter Type 4
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Insulin / pharmacology*
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Interleukin-1 / pharmacology
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Interleukin-6 / pharmacology
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Lymphokines / pharmacology
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Mice
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Monosaccharide Transport Proteins / analysis
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Monosaccharide Transport Proteins / genetics
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Muscle Proteins*
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Thiazoles / pharmacology*
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Thiazolidinediones*
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Transcription Factor AP-1 / analysis
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Transcription Factor AP-1 / genetics
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Transforming Growth Factor beta / pharmacology
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Troglitazone
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Blood Glucose
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Chromans
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Cytokines
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Glucose Transporter Type 4
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Insulin
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Interleukin-1
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Interleukin-6
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Lymphokines
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Monosaccharide Transport Proteins
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Muscle Proteins
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Slc2a4 protein, mouse
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Thiazoles
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Thiazolidinediones
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Transcription Factor AP-1
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Transforming Growth Factor beta
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Tumor Necrosis Factor-alpha
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leukocyte inhibitory factor
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Troglitazone
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Glucose