PMID- 27082050
OWN - NLM
STAT- MEDLINE
DCOM- 20170228
LR  - 20170228
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 37
IP  - 6
DP  - 2016 Jun
TI  - Astragaloside IV facilitates glucose transport in C2C12 myotubes through the 
      IRS1/AKT pathway and suppresses the palmitate-induced activation of the IKK/IkappaBalpha 
      pathway.
PG  - 1697-705
LID - 10.3892/ijmm.2016.2555 [doi]
AB  - Astragaloside IV is a monomer isolated from Astragalus membranaceus (Fisch.) 
      Bunge, which is one of the most widely used plant-derived drugs in traditional 
      Chinese medicine for diabetes therapy. In the present study, we aimed to examine 
      the effects of astragaloside IV on glucose in C2C12 myotubes and the underlying 
      molecular mechanisms responsible for these effects. Four-day differentiated C2C12 
      myotubes were exposed to palmitate for 16 h in order to establish a model of 
      insulin resistance and 3H glucose uptake, using 
      2-Deoxy‑D‑[1,2-3H(N)]-glucose (radiolabeled 2-DG), was detected. Astragaloside IV 
      was added 2 h prior to palmitate exposure. The translocation of glucose 
      transporter 4 (GLUT4) was evaluated by subcellular fractionation, and the 
      expression of insulin signaling molecules such as insulin receptor beta (IRbeta), 
      insulin receptor substrate (IRS)1/protein kinase B (AKT) and inhibitory kappaB 
      kinase (IKK)/inhibitor-kappaBalpha (IkappaBalpha), which are associated with insulin signal 
      transduction, were assessed in the basal or the insulin‑stimulated state using 
      western blot analysis or RT-PCR. We also examined the mRNA expression of monocyte 
      chemotactic protein 1 (MCP-1), interleukin 6 (IL-6), tumor necrosis 
      factor alpha (TNFalpha) and Toll‑like receptor 4 (TLR4). Taken together, these findings 
      demonstrated that astragaloside IV facilitates glucose transport in C2C12 
      myotubes through a mechanism involving the IRS1/AKT pathway, and suppresses the 
      palmitate-induced activation of the IKK/IkappaBalpha pathway.
FAU - Zhu, Rongfeng
AU  - Zhu R
AD  - Department of Internal Medicine, The 95th Hospital of Chinese People's Liberation 
      Army, Putian, Fujian 351100, P.R. China.
FAU - Zheng, Jianjun
AU  - Zheng J
AD  - Department of Internal Medicine, The 95th Hospital of Chinese People's Liberation 
      Army, Putian, Fujian 351100, P.R. China.
FAU - Chen, Lizhen
AU  - Chen L
AD  - Department of Internal Medicine, The 95th Hospital of Chinese People's Liberation 
      Army, Putian, Fujian 351100, P.R. China.
FAU - Gu, Bin
AU  - Gu B
AD  - Department of Internal Medicine, The 95th Hospital of Chinese People's Liberation 
      Army, Putian, Fujian 351100, P.R. China.
FAU - Huang, Shengli
AU  - Huang S
AD  - Department of Internal Medicine, The 95th Hospital of Chinese People's Liberation 
      Army, Putian, Fujian 351100, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20160411
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 0 (Interleukin-6)
RN  - 0 (Irs1 protein, mouse)
RN  - 0 (Saponins)
RN  - 0 (Slc2a4 protein, mouse)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Triterpenes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (interleukin-6, mouse)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - 3A592W8XKE (astragaloside A)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Biological Transport/drug effects
MH  - Cell Line
MH  - Chemokine CCL2/genetics/metabolism
MH  - Gene Expression Regulation/*drug effects
MH  - Glucose/*agonists/metabolism
MH  - Glucose Transporter Type 4/genetics/metabolism
MH  - Hypoglycemic Agents/*pharmacology
MH  - I-kappa B Kinase/genetics/metabolism
MH  - Insulin Receptor Substrate Proteins/genetics/metabolism
MH  - Insulin Resistance
MH  - Interleukin-6/genetics/metabolism
MH  - Mice
MH  - Models, Biological
MH  - Muscle Fibers, Skeletal/cytology/*drug effects/metabolism
MH  - NF-KappaB Inhibitor alpha/genetics/metabolism
MH  - Palmitic Acid/*antagonists & inhibitors/pharmacology
MH  - Proto-Oncogene Proteins c-akt/genetics/metabolism
MH  - Saponins/*pharmacology
MH  - Signal Transduction
MH  - Toll-Like Receptor 4/genetics/metabolism
MH  - Triterpenes/*pharmacology
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 2016/04/16 06:00
MHDA- 2017/03/01 06:00
CRDT- 2016/04/16 06:00
PHST- 2015/12/17 00:00 [received]
PHST- 2016/03/29 00:00 [accepted]
PHST- 2016/04/16 06:00 [entrez]
PHST- 2016/04/16 06:00 [pubmed]
PHST- 2017/03/01 06:00 [medline]
AID - 10.3892/ijmm.2016.2555 [doi]
PST - ppublish
SO  - Int J Mol Med. 2016 Jun;37(6):1697-705. doi: 10.3892/ijmm.2016.2555. Epub 2016 
      Apr 11.