PMID- 22653991
OWN - NLM
STAT- MEDLINE
DCOM- 20130108
LR  - 20211021
IS  - 1522-1601 (Electronic)
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 113
IP  - 3
DP  - 2012 Aug
TI  - Diminished muscle growth in the obese Zucker rat following overload is associated 
      with hyperphosphorylation of AMPK and dsRNA-dependent protein kinase.
PG  - 377-84
LID - 10.1152/japplphysiol.00397.2011 [doi]
AB  - Previous data have suggested that insulin-resistant skeletal muscle may exhibit a 
      diminished ability to undergo hypertrophy and that this result may be mediated, 
      at least in part, from decrements in mammalian target of rapamycin (mTOR) 
      signaling (Katta A, Kundla S, Kakarla SK, Wu M, Fannin J, Paturi S, Liu H, 
      Addagarla HS, Blough ER. Am J Physiol Regul Integr Comp Physiol 299: R1666-R1675, 
      2010). Herein, we attempt to extend these observations by determining if this 
      attenuation in muscle growth is associated with alterations in AMP-activated 
      protein kinase (AMPK) signaling, an upstream mediator of mTOR, and changes in the 
      activation of dsRNA-dependent protein kinase (PKR), which functions as an 
      inhibitor of protein synthesis and potential mediator of protein degradation. 
      Compared with that observed in lean Zucker (LZ) rats, the phosphorylation of 
      AMPKalpha at Thr172 was higher after 3 wk of overload in the insulin-resistant obese 
      Zucker (OZ) soleus (P < 0.05). This change in AMPKalpha phosphorylation was 
      accompanied by increases in the amount of phosphorylated PKR (Thr446), elevations 
      in the PKR-dependent phosphorylation of eukaryotic initiation factor (eIF)-2alpha 
      (Ser51), augmented p38 MAP kinase (Thr180/Tyr182) phosphorylation, and increases 
      in the amount of protein ubiquitination (P < 0.05). Taken together, these results 
      suggest that the diminished hypertrophic response we observe in the OZ rat may be 
      mediated, at least in part, by the hyperactivation of AMPK- and PKR-related 
      signaling.
FAU - Katta, Anjaiah
AU  - Katta A
AD  - Center for Diagnostic Nanosystems, Marshall University, Huntington, WV 
      25755-1090, USA.
FAU - Kakarla, Sunil K
AU  - Kakarla SK
FAU - Manne, Nandini D P K
AU  - Manne ND
FAU - Wu, Miaozong
AU  - Wu M
FAU - Kundla, Sudarsanam
AU  - Kundla S
FAU - Kolli, Madhukar B
AU  - Kolli MB
FAU - Nalabotu, Siva K
AU  - Nalabotu SK
FAU - Blough, Eric R
AU  - Blough ER
LA  - eng
GR  - AG-027103-1/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20120531
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 2ZD004190S (Threonine)
RN  - 42HK56048U (Tyrosine)
RN  - 452VLY9402 (Serine)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Animals
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Insulin Resistance/physiology
MH  - Male
MH  - Muscle, Skeletal/enzymology/*growth & development
MH  - Obesity/enzymology/*physiopathology
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Zucker
MH  - Serine/metabolism
MH  - Signal Transduction/physiology
MH  - Threonine/metabolism
MH  - Tyrosine/metabolism
MH  - Ubiquitination/physiology
MH  - eIF-2 Kinase/*metabolism
PMC - PMC3426165
EDAT- 2012/06/02 06:00
MHDA- 2013/01/09 06:00
PMCR- 2013/08/01
CRDT- 2012/06/02 06:00
PHST- 2012/06/02 06:00 [entrez]
PHST- 2012/06/02 06:00 [pubmed]
PHST- 2013/01/09 06:00 [medline]
PHST- 2013/08/01 00:00 [pmc-release]
AID - japplphysiol.00397.2011 [pii]
AID - JAPPL-00397-2011 [pii]
AID - 10.1152/japplphysiol.00397.2011 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2012 Aug;113(3):377-84. doi: 
      10.1152/japplphysiol.00397.2011. Epub 2012 May 31.