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

Title
Tanshinone IIA improves endoplasmic reticulum stress-induced insulin resistance through AMP-activated protein kinase
Author(s)
장현욱황승락양주혜정용태김용덕[김용덕]이선유예장영채[장영채]손건호[손건호]
Keywords
SKELETAL-MUSCLE; GLUCOSE-UPTAKE; SALVIA-MILTIORRHIZA; SIGNALING PATHWAYS; RAW-264.7 CELLS; ER STRESS; CONTRACTION; TRANSPORT; MICE; LKB1
Issue Date
201301
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.430, no.4, pp.1246 - 1252
Abstract
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. (C) 2012 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/26836http://dx.doi.org/10.1016/j.bbrc.2012.12.066
ISSN
0006-291X
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약학대학 > 약학부 > Articles
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