CIDeRGeneral Information:
| Id: | 1,467 (click here to show other Interactions for entry) |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Homo sapiens | |
| BTO:0000599 Hep-G2 cell | |
| article | |
| Reference: | Kim JH et al.(2008) Regulation of interleukin-6-induced hepatic insulin resistance by mammalian target of rapamycin through the STAT3-SOCS3 pathway J. Biol. Chem. 283: 708-715 [PMID: 17993646] |
Interaction Information:
| Comment | Pre-treatment of serum-starved HepG2 cells (a frequently untilized in vitro system for studying insulin's effects on hepatic cells) by IL-6 significantly dampened their response to acute insulin stimulation, as measured by Akt phosphorylation at Ser473. |
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Formal Description Interaction-ID: 10356 |
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| Drugbank entries | Show/Hide entries for IL6 |
| Comment | IL-6 activates S6K1 in HepG2 hepatocarcinoma cells, but unexpectedly, S6K1 is not involved in IL-6 inhibition of insulin signaling, since the effect of IL-6 persists in cells with drastically reduced S6K1 levels induced by RNA interference, suggesting that the function of mTOR signaling is through a mechanism different from the prevailing model of S6K1 phosphorylation of insulin receptor substrate-1. |
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Formal Description Interaction-ID: 10441 |
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| Comment | Phosphorylation of STAT3 on Ser(727) and STAT3 transcriptional activity are regulated by mTOR upon IL-6 stimulation and STAT3 is required for IL-6 inhibition of insulin signaling. |
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Formal Description Interaction-ID: 10445 |
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| Comment | IL-6-induced SOCS3 expression is inhibited by rapamycin, and ectopic expression of SOCS3 blocks the ability of rapamycin to enhance insulin sensitivity in the presence of IL-6. SOCS3 mediates the role of mTOR in the IL-6 inhibition of insulin signaling. |
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Formal Description Interaction-ID: 10449 |
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