Lipopolysaccharide impairs insulin sensitivity via activation of phosphoinositide 3-kinase in adipocytes. (April 2014)

• Record Type: Journal Article
• Authors: Wakayama, Sayori; Haque, Abedul; Koide, Naoki; Kato, Yoshiro; Odkhuu, Erdenezaya; Bilegtsaikhan, Tsolmongyn; Naiki, Yoshikazu; Komatsu, Takayuki; Yoshida, Tomoaki; Yokochi, Takashi
• Is Part Of: Immunopharmacology and immunotoxicology. Volume 36:Number 2(2014:Apr.)
• Page Start: 145
• Page End: 149
• Publication Date: 2014-04
• Subjects: Immunopharmacology -- Periodicals; Immunotoxicology -- Periodicals; Antibody-toxin conjugates -- Periodicals; Immunology -- Periodicals; 615.37
• DOI: 10.3109/08923973.2014.887096
• Languages: English
• ISSNs: 0892-3973

Abstract

<abstract> <title>Abstract</title> <p>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.</p> </abstract>