PMID- 24454989
OWN - NLM
STAT- MEDLINE
DCOM- 20140715
LR  - 20211021
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2013
DP  - 2013
TI  - Astragalus polysaccharide suppresses skeletal muscle myostatin expression in 
      diabetes: involvement of ROS-ERK and NF-kappaB pathways.
PG  - 782497
LID - 10.1155/2013/782497 [doi]
LID - 782497
AB  - OBJECTIVE: The antidiabetes drug astragalus polysaccharide (APS) is capable of 
      increasing insulin sensitivity in skeletal muscle and improving whole-body 
      glucose homeostasis. Recent studies suggest that skeletal muscle secreted growth 
      factor myostatin plays an important role in regulating insulin signaling and 
      insulin resistance. We hypothesized that regulation of skeletal muscle myostatin 
      expression may be involved in the improvement of insulin sensitivity by APS. 
      METHODS: APS was administered to 13-week-old diabetic KKAy and nondiabetic 
      C57BL/6J mice for 8 weeks. Complementary studies examined APS effects on the 
      saturated acid palmitate-induced insulin resistance and myostatin expression in 
      C2C12 cells. RESULTS: APS treatment ameliorated hyperglycemia, hyperlipidemia, 
      and insulin resistance and decreased the elevation of myostatin expression and 
      malondialdehyde production in skeletal muscle of noninsulin-dependent diabetic 
      KKAy mice. In C2C12 cells in vitro, saturated acid palmitate-induced impaired 
      glucose uptake, overproduction of ROS, activation of extracellular regulated 
      protein kinases (ERK), and NF-kappaB were partially restored by APS treatment. The 
      protective effects of APS were mimicked by ERK and NF-kappaB inhibitors, 
      respectively. CONCLUSION: Our study demonstrates elevated myostatin expression in 
      skeletal muscle of type 2 diabetic KKAy mice and in cultured C2C12 cells exposed 
      to palmitate. APS is capable of improving insulin sensitivity and decreasing 
      myostatin expression in skeletal muscle through downregulating ROS-ERK-NF-kappaB 
      pathway.
FAU - Liu, Min
AU  - Liu M
AD  - Department of Pathology and Pathophysiology, School of Medicine, Wuhan 
      University, Wuhan 430071, China ; Central Laboratory, Renmin Hospital of Wuhan 
      University, Wuhan 430060, China.
FAU - Qin, Jian
AU  - Qin J
AD  - Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
FAU - Hao, Yarong
AU  - Hao Y
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, 
      China.
FAU - Liu, Min
AU  - Liu M
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, 
      China.
FAU - Luo, Jun
AU  - Luo J
AD  - Department of Pathology, Zhongnan Hospital of Wuhan University, Wuhan 430071, 
      China.
FAU - Luo, Tao
AU  - Luo T
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, 
      China.
FAU - Wei, Lei
AU  - Wei L
AD  - Department of Pathology and Pathophysiology, School of Medicine, Wuhan 
      University, Wuhan 430071, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131218
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Blood Glucose)
RN  - 0 (Fatty Acids)
RN  - 0 (Myostatin)
RN  - 0 (NF-kappa B)
RN  - 0 (Polysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Body Weight/drug effects
MH  - Cell Line
MH  - Diabetes Mellitus, Experimental/blood/enzymology/*metabolism/pathology
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Fatty Acids/blood
MH  - Gene Expression Regulation/drug effects
MH  - Insulin Resistance
MH  - MAP Kinase Signaling System/drug effects
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Muscle, Skeletal/drug effects/*metabolism
MH  - Myostatin/genetics/*metabolism
MH  - NF-kappa B/*metabolism
MH  - Palmitic Acid/pharmacology
MH  - Polysaccharides/*pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Reactive Oxygen Species/*metabolism
PMC - PMC3880770
EDAT- 2014/01/24 06:00
MHDA- 2014/07/16 06:00
PMCR- 2013/12/18
CRDT- 2014/01/24 06:00
PHST- 2013/08/07 00:00 [received]
PHST- 2013/10/24 00:00 [revised]
PHST- 2013/10/27 00:00 [accepted]
PHST- 2014/01/24 06:00 [entrez]
PHST- 2014/01/24 06:00 [pubmed]
PHST- 2014/07/16 06:00 [medline]
PHST- 2013/12/18 00:00 [pmc-release]
AID - 10.1155/2013/782497 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2013;2013:782497. doi: 10.1155/2013/782497. Epub 2013 Dec 
      18.