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Immunopharmacol Immunotoxicol ; 36(2): 145-9, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24506665

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.


Subject(s)
Adipocytes/drug effects , Insulin Resistance/physiology , Insulin/metabolism , Lipopolysaccharides/pharmacology , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , 3T3-L1 Cells , Adipocytes/metabolism , Animals , Cell Line , Glycogen Synthase Kinase 3/metabolism , Insulin Receptor Substrate Proteins/metabolism , Mice , Signal Transduction/drug effects , Suppressor of Cytokine Signaling 3 Protein , Suppressor of Cytokine Signaling Proteins/metabolism
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