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Publication : Tanshinone IIA improves endoplasmic reticulum stress-induced insulin resistance through AMP-activated protein kinase.

First Author  Hwang SL Year  2013
Journal  Biochem Biophys Res Commun Volume  430
Issue  4 Pages  1246-52
PubMed ID  23266607 Mgi Jnum  J:193843
Mgi Id  MGI:5469773 Doi  10.1016/j.bbrc.2012.12.066
Citation  Hwang SL, et al. (2013) Tanshinone IIA improves endoplasmic reticulum stress-induced insulin resistance through AMP-activated protein kinase. Biochem Biophys Res Commun 430(4):1246-52
abstractText  The aim of the present study was to determine the effect of Tanshinone IIA (Tan IIA) on endoplasmic reticulum (ER) stress-induced insulin resistance in L6 myotubes and db/db mice. ER stress markers, RNA-activated protein kinase-like ER resident kinase (PERK), JNK, and AMPK activity were determined in tunicamycin-treated L6 myotubes. Insulin resistance was monitored using glucose uptake assays in vitro and blood glucose levels in vivo. Tan IIA clearly suppressed the phosphorylations of PERK and JNK and potentiated insulin-mediated Akt phosphorylation as well as glucose uptake via AMPK activation under ER stress. Furthermore, these effects are completely abrogated by siRNA-mediated knockdown of AMPK or LKB1. In addition, Tan IIA reduced blood glucose levels and body weights in db/db mice without altering food intake. These findings suggest that Tan IIA enhances insulin sensitivity and improves glucose metabolic disorders by increasing AMPK activity and attenuating ER stress-induced insulin resistance.
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