PMID- 24204984
OWN - NLM
STAT- MEDLINE
DCOM- 20140904
LR  - 20211203
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 10
DP  - 2013
TI  - Essential amino acid enriched high-protein enteral nutrition modulates 
      insulin-like growth factor-1 system function in a rat model of trauma-hemorrhagic 
      shock.
PG  - e77823
LID - 10.1371/journal.pone.0077823 [doi]
LID - e77823
AB  - BACKGROUND: Nutrition support for critically ill patients supplemented with 
      additional modular protein may promote skeletal muscle protein anabolism in 
      addition to counteracting acute nitrogen loss. The present study was designed to 
      investigate whether the essential amino acid (EAA) enriched high-protein enteral 
      nutrition (EN) modulates the insulin-like growth factor-1 (IGF-1) system and 
      activates the mammalian target of rapamycin (mTOR) anabolic signaling pathway in 
      a trauma-hemorrhagic shock (T-HS) rat model. METHODOLOGY/PRINCIPAL FINDINGS: Male 
      Sprague-Dawley rats (n = 90, 278.18 +/- 0.94 g) were randomly assigned to 5 groups: 
      (1) normal control, (2) pair-fed, (3) T-HS, (4) T-HS and standard EN, and (5) 
      T-HS and EAA enriched high-protein EN. Six animals from each group were harvested 
      on days 2, 4, and 6 for serum, gastrocnemius, soleus, and extensor digitorum 
      longus sample collection. T-HS significantly reduced muscle mass. Nutrition 
      support maintained muscle mass, especially the EAA enriched high-protein EN. 
      Meanwhile, a pronounced derangement in IGF-1-IGFBPs axis as well as impaired mTOR 
      transduction was observed in the T-HS group. Compared with animals receiving 
      standard EN, those receiving EAA enriched high-protein EN presented 18% higher 
      serum free IGF-1 levels following 3 days of nutrition support and 22% higher 
      after 5 days. These changes were consistent with the concomitant elevation in 
      serum insulin and reduction in corticosterone levels. In addition, 
      phosphorylations of downstream anabolic signaling effectors - including protein 
      kinase B, mTOR, and ribosomal protein S6 kinase1 - increased significantly in 
      rats receiving EAA enriched high-protein EN. CONCLUSION/SIGNIFICANCE: Our 
      findings firstly demonstrate the beneficial effect of EAA enriched high-protein 
      EN on the metabolic modulation of skeletal muscle protein anabolism by regulating 
      the IGF-1 system and downstream anabolic signaling transduction.
FAU - Xia, Xianfeng
AU  - Xia X
AD  - Research Institute of General Surgery, Jinling Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu Province, China.
FAU - Wang, Xinying
AU  - Wang X
FAU - Li, Qiurong
AU  - Li Q
FAU - Li, Ning
AU  - Li N
FAU - Li, Jieshou
AU  - Li J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131028
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Amino Acids, Essential)
RN  - 0 (Dietary Proteins)
RN  - 0 (Insulin)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Amino Acids, Essential/*administration & dosage
MH  - Animals
MH  - Blotting, Western
MH  - Corticosterone/blood
MH  - Dietary Proteins/*administration & dosage
MH  - *Disease Models, Animal
MH  - *Enteral Nutrition
MH  - Insulin/blood
MH  - Insulin-Like Growth Factor I/*metabolism
MH  - Male
MH  - Muscle, Skeletal/metabolism/pathology
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Shock, Hemorrhagic/*metabolism/pathology/therapy
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/blood
MH  - Wounds and Injuries/*metabolism/pathology/therapy
PMC - PMC3810136
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/11/10 06:00
MHDA- 2014/09/05 06:00
PMCR- 2013/10/28
CRDT- 2013/11/09 06:00
PHST- 2013/06/10 00:00 [received]
PHST- 2013/09/04 00:00 [accepted]
PHST- 2013/11/09 06:00 [entrez]
PHST- 2013/11/10 06:00 [pubmed]
PHST- 2014/09/05 06:00 [medline]
PHST- 2013/10/28 00:00 [pmc-release]
AID - PONE-D-13-23948 [pii]
AID - 10.1371/journal.pone.0077823 [doi]
PST - epublish
SO  - PLoS One. 2013 Oct 28;8(10):e77823. doi: 10.1371/journal.pone.0077823. 
      eCollection 2013.