Abstract：
:The contribution of interleukin (IL)-6 signaling in obesity-induced inflammation remains controversial. To specifically define the role of hepatic IL-6 signaling in insulin action and resistance, we have generated mice with hepatocyte-specific IL-6 receptor (IL-6R) alpha deficiency (IL-6Ralpha(L-KO) mice). These animals showed no alterations in body weight and fat content but exhibited a reduction in insulin sensitivity and glucose tolerance. Impaired glucose metabolism originated from attenuated insulin-stimulated glucose transport in skeletal muscle and fat. Surprisingly, hepatic IL-6Ralpha-disruption caused an exaggerated inflammatory response during euglycemic hyperinsulinemic clamp analysis, as revealed by increased expression of IL-6, TNF-alpha, and IL-10, as well as enhanced activation of inflammatory signaling such as phosphorylation of IkappaBalpha. Neutralization of TNF-alpha or ablation of Kupffer cells restored glucose tolerance in IL-6Ralpha(L-KO) mice. Thus, our results reveal an unexpected role for hepatic IL-6 signaling to limit hepatic inflammation and to protect from local and systemic insulin resistance.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Wunderlich FT,Ströhle P,Könner AC,Gruber S,Tovar S,Brönneke HS,Juntti-Berggren L,Li LS,van Rooijen N,Libert C,Berggren PO,Brüning JCdoi
10.1016/j.cmet.2010.06.011subject
Has Abstractpub_date
2010-09-08 00:00:00pages
237-49issue
3eissn
1550-4131issn
1932-7420pii
S1550-4131(10)00271-8journal_volume
12pub_type
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