TY - JOUR
T1 - Lipopolysaccharide impairs insulin sensitivity via activation of phosphoinositide 3-kinase in adipocytes
AU - Wakayama, Sayori
AU - Haque, Abedul
AU - Koide, Naoki
AU - Kato, Yoshiro
AU - Odkhuu, Erdenezaya
AU - Bilegtsaikhan, Tsolmongyn
AU - Naiki, Yoshikazu
AU - Komatsu, Takayuki
AU - Yoshida, Tomoaki
AU - Yokochi, Takashi
N1 - Funding Information:
This work was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan and a grant of MEXT-Supported Program for the Strategic Research Foundation at Private Universities, 2011–2015(S1101027).
PY - 2014/4
Y1 - 2014/4
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/84897851289
UR - https://www.scopus.com/pages/publications/84897851289#tab=citedBy
U2 - 10.3109/08923973.2014.887096
DO - 10.3109/08923973.2014.887096
M3 - Article
C2 - 24506665
AN - SCOPUS:84897851289
SN - 0892-3973
VL - 36
SP - 145
EP - 149
JO - Immunopharmacology and Immunotoxicology
JF - Immunopharmacology and Immunotoxicology
IS - 2
ER -