PMID- 25057926
OWN - NLM
STAT- MEDLINE
DCOM- 20150812
LR  - 20211203
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 43
IP  - 1
DP  - 2015 Jan
TI  - Extracellular signal-regulated kinase-mammalian target of rapamycin signaling and 
      forkhead-box transcription factor 3a phosphorylation are involved in 
      testosterone's effect on severe burn injury in a rat model.
PG  - 85-91
LID - 10.1097/SHK.0000000000000244 [doi]
AB  - BACKGROUND: Testosterone and androgen receptor agonists have been known for a 
      long time to prevent or reverse muscle wasting in burn injury patients, but the 
      exact molecular mechanisms are not clear. OBJECTIVE: To investigate the 
      underlying molecular mechanisms of testosterone in severely burned rats. METHODS: 
      Severe burn injuries were induced by immersing the back of the rat in 100  degrees C 
      water for 12 s. Rats were treated for 14 days with vehicle (burn group) or a 
      physiological replacement dose of testosterone (B + T group) immediately after 
      injury. Gene and protein expressions were assessed by real-time polymerase chain 
      reaction and Western blot. RESULTS: Testosterone improved glucose metabolism, 
      reduced body weight loss, and attenuated tibialis anterior muscle mass loss and 
      muscle protein breakdown. In rat tibialis anterior muscle, testosterone 
      positively regulated the insulin-sensitive glucose transporters Glut3 and Glut4 
      genes and glycogen synthase 1 protein. These changes would be expected to improve 
      glucose metabolism and nutrient availability in skeletal muscle. Administration 
      of testosterone negatively regulated atrogin 1 (Fbxo32) by increasing total and 
      phosphorylated Foxo3a (forkhead-box transcription factor 3a) levels and 
      positively regulated the expression of the mammalian target of rapamycin (mTOR) 
      and its downstream proteins p70S6 and S6 through mTOR-extracellular 
      signal-regulated kinase phosphorylation. CONCLUSIONS: RESULTS suggested that 
      testosterone might regulate skeletal muscle glucose and protein metabolism 
      following burn injury in part by affecting extracellular signal-regulated 
      kinase-mTOR signaling and Foxo3a levels.
FAU - Ma, Li
AU  - Ma L
AD  - Department of Burns and Plastic Surgery, Burns Institute, First Hospital 
      Affiliated to General Hospital of PLA, Beijing, China.
FAU - Shen, Chuanan
AU  - Shen C
FAU - Chai, Jiake
AU  - Chai J
FAU - Yin, Huinan
AU  - Yin H
FAU - Deng, Huping
AU  - Deng H
FAU - Feng, Rui
AU  - Feng R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Androgens)
RN  - 0 (FOXO3 protein, rat)
RN  - 0 (Forkhead Box Protein O3)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Glucose Transporter Type 3)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Slc2a3 protein, rat)
RN  - 0 (Slc2a4 protein, rat)
RN  - 3XMK78S47O (Testosterone)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Androgens/*pharmacology
MH  - Animals
MH  - Burns/*metabolism/pathology
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Forkhead Box Protein O3
MH  - Forkhead Transcription Factors/*metabolism
MH  - Glucose/metabolism
MH  - Glucose Transporter Type 3/metabolism
MH  - Glucose Transporter Type 4/metabolism
MH  - MAP Kinase Signaling System/*drug effects
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Ribosomal Protein S6 Kinases, 70-kDa/metabolism
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Testosterone/*pharmacology
EDAT- 2014/07/25 06:00
MHDA- 2015/08/13 06:00
CRDT- 2014/07/25 06:00
PHST- 2014/07/25 06:00 [entrez]
PHST- 2014/07/25 06:00 [pubmed]
PHST- 2015/08/13 06:00 [medline]
AID - 10.1097/SHK.0000000000000244 [doi]
PST - ppublish
SO  - Shock. 2015 Jan;43(1):85-91. doi: 10.1097/SHK.0000000000000244.