Abstract
The effect of lipopolysaccharide (LPS) on insulin sensitivity in adipocytes were examined by using differentiated 3T3-L1 adipocytes. Insulin-mediated activation of insulin receptor substrate (IRS) 1/2 was inhibited in LPS-pretreated adipocytes and IRS1/2-mediated Akt activation was also attenuated in those cells. LPS inhibited activation of glycogen synthase kinase 3 as a negative regulator of glycogenesis and impaired the glycogen synthesis in response to insulin. LPS-induced activation of phosphoinositide 3-kinase (PI3K) in adipocytes. Involvement of suppressor of cytokine signaling 3 (SOCS3) in LPS-induced IRS1/2 inhibition was excluded. Considering that both insulin and LPS were able to activate the PI3K/Akt signaling pathway, LPS was suggested to impair insulin sensitivity of adipocytes through down-regulating insulin-mediated PI3K/Akt activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3-L1 Cells
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Adipocytes / drug effects*
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Adipocytes / metabolism
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Animals
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Cell Line
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Glycogen Synthase Kinase 3 / metabolism
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Insulin / metabolism*
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Insulin Receptor Substrate Proteins / metabolism
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Insulin Resistance / physiology*
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Lipopolysaccharides / pharmacology*
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Mice
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Phosphatidylinositol 3-Kinases / metabolism*
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Proto-Oncogene Proteins c-akt / metabolism*
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Signal Transduction / drug effects
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Suppressor of Cytokine Signaling 3 Protein
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Suppressor of Cytokine Signaling Proteins / metabolism
Substances
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Insulin
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Insulin Receptor Substrate Proteins
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Irs1 protein, mouse
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Irs2 protein, mouse
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Lipopolysaccharides
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Socs3 protein, mouse
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Suppressor of Cytokine Signaling 3 Protein
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Suppressor of Cytokine Signaling Proteins
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Phosphatidylinositol 3-Kinases
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Proto-Oncogene Proteins c-akt
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Glycogen Synthase Kinase 3