Lipopolysaccharide impairs insulin sensitivity via activation of phosphoinositide 3-kinase in adipocytes

被引：2

作者：

Wakayama, Sayori ^{[1
]}

Haque, Abedul ^{[1
]}

Koide, Naoki ^{[1
]}

Kato, Yoshiro ^{[2
]}

Odkhuu, Erdenezaya ^{[1
]}

Bilegtsaikhan, Tsolmongyn ^{[1
]}

Naiki, Yoshikazu ^{[1
]}

Komatsu, Takayuki ^{[1
]}

Yoshida, Tomoaki ^{[1
]}

Yokochi, Takashi ^{[1
]}

机构：

[1] Aichi Med Univ, Sch Med, Dept Microbiol & Immunol, Nagakute, Aichi 4801195, Japan

[2] Aichi Med Univ, Sch Med, Div Diabet, Dept Internal Med, Nagakute, Aichi 4801195, Japan

来源：

IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY | 2014年 / 36卷 / 02期

关键词：

Adipocytes; insulin receptor substrate; insulin sensitivity; lipopolysaccharide; phosphoinositide; 3-kinase; GLYCOGEN-SYNTHASE KINASE-3; KAPPA-B ACTIVATION; MOLECULAR-MECHANISMS; ALVEOLAR MACROPHAGES; INDUCED INFLAMMATION; SIGNALING SYSTEM; NITRIC-OXIDE; RESISTANCE; RECEPTOR; LPS;

D O I：

10.3109/08923973.2014.887096

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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 (P13K) 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 P13K/Akt signaling pathway, LPS was suggested to impair insulin sensitivity of adipocytes through down-regulating insulin-mediated P13K/Akt activation.

引用

页码：145 / 149

页数：5

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