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. 2018 Oct 16;9:1180. doi: 10.3389/fphar.2018.01180

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Copyright © 2018 Li, Zhang, Cao, Zhang, Liu, Guo and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram of icariin regulation upon PA-induced insulin resistance. Proteasome functions as a key role in PA-induced insulin resistance in C2C12 myotubes. Dysfunction of proteasome facilitates ER stress and promotes an increase of TXNIP protein levels. Excessive TXNIP contributes to inflammatory response and hyperactivation of STAT3 leading to insulin resistance. In addition, ER stress induces insulin resistance through inflammation and JNK/IRS-1 pathway. The precise mechanism that regulates proteasome remains unclear; however, the improvement of proteasome activity by icariin administration results in degradation of TXNIP protein and attenuation of ER stress, both of which contribute to improvement of insulin resistance.