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Immunopharmacol Immunotoxicol ; 36(2): 145-9, 2014 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-24506665

RESUMEN

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.


Asunto(s)
Adipocitos/efectos de los fármacos , Resistencia a la Insulina/fisiología , Insulina/metabolismo , Lipopolisacáridos/farmacología , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Células 3T3-L1 , Adipocitos/metabolismo , Animales , Línea Celular , Glucógeno Sintasa Quinasa 3/metabolismo , Proteínas Sustrato del Receptor de Insulina/metabolismo , Ratones , Transducción de Señal/efectos de los fármacos , Proteína 3 Supresora de la Señalización de Citocinas , Proteínas Supresoras de la Señalización de Citocinas/metabolismo
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