PMID- 26758685
OWN - NLM
STAT- MEDLINE
DCOM- 20160802
LR  - 20211203
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 310
IP  - 6
DP  - 2016 Mar 15
TI  - AMPKgamma3 is dispensable for skeletal muscle hypertrophy induced by functional 
      overload.
PG  - E461-72
LID - 10.1152/ajpendo.00387.2015 [doi]
AB  - Mechanisms regulating skeletal muscle growth involve a balance between the 
      activity of serine/threonine protein kinases, including the mammalian target of 
      rapamycin (mTOR) and 5'-AMP-activated protein kinase (AMPK). The contribution of 
      different AMPK subunits to the regulation of cell growth size remains 
      inadequately characterized. Using AMPKgamma3 mutant-overexpressing transgenic 
      Tg-Prkag3(225Q) and AMPKgamma3-knockout (Prkag3(-/-)) mice, we investigated the 
      requirement for the AMPKgamma3 isoform in functional overload-induced muscle 
      hypertrophy. Although the genetic disruption of the gamma3 isoform did not impair 
      muscle growth, control sham-operated AMPKgamma3-transgenic mice displayed heavier 
      plantaris muscles in response to overload hypertrophy and underwent smaller mass 
      gain and lower Igf1 expression compared with wild-type littermates. The mTOR 
      signaling pathway was upregulated with functional overload but unchanged between 
      genetically modified animals and wild-type littermates. Differences in 
      AMPK-related signaling pathways between transgenic, knockout, and wild-type mice 
      did not impact muscle hypertrophy. Glycogen content was increased following 
      overload in wild-type mice. In conclusion, our functional, transcriptional, and 
      signaling data provide evidence against the involvement of the AMPKgamma3 isoform in 
      the regulation of skeletal muscle hypertrophy. Thus, the AMPKgamma3 isoform is 
      dispensable for functional overload-induced muscle growth. Mechanical loading can 
      override signaling pathways that act as negative effectors of mTOR signaling and 
      consequently promote skeletal muscle hypertrophy.
CI  - Copyright (c) 2016 the American Physiological Society.
FAU - Riedl, Isabelle
AU  - Riedl I
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden;
FAU - Osler, Megan E
AU  - Osler ME
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden;
FAU - Bjornholm, Marie
AU  - Bjornholm M
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden;
FAU - Egan, Brendan
AU  - Egan B
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden; Institute for Sport and Health, School of Public Health, Physiotherapy, 
      and Population Science, University College Dublin, Belfield, Dublin, Ireland.
FAU - Nader, Gustavo A
AU  - Nader GA
AD  - Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, 
      Sweden; and.
FAU - Chibalin, Alexander V
AU  - Chibalin AV
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden;
FAU - Zierath, Juleen R
AU  - Zierath JR
AD  - Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, 
      Sweden; Department of Physiology and Pharmacology, Karolinska Institutet, 
      Stockholm, Sweden; and Juleen.Zierath@ki.se.
LA  - eng
GR  - P30 DK020541/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160112
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (insulin-like growth factor-1, mouse)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (Prkag3 protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*genetics
MH  - Animals
MH  - Hypertrophy/genetics
MH  - Insulin-Like Growth Factor I/*metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Muscle, Skeletal/*growth & development/metabolism
MH  - Organ Size
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC4796264
OTO - NOTNLM
OT  - AMP-activated protein kinase-gamma3
EDAT- 2016/01/14 06:00
MHDA- 2016/08/03 06:00
PMCR- 2017/03/15
CRDT- 2016/01/14 06:00
PHST- 2015/08/26 00:00 [received]
PHST- 2016/01/06 00:00 [accepted]
PHST- 2016/01/14 06:00 [entrez]
PHST- 2016/01/14 06:00 [pubmed]
PHST- 2016/08/03 06:00 [medline]
PHST- 2017/03/15 00:00 [pmc-release]
AID - ajpendo.00387.2015 [pii]
AID - E-00387-2015 [pii]
AID - 10.1152/ajpendo.00387.2015 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2016 Mar 15;310(6):E461-72. doi: 
      10.1152/ajpendo.00387.2015. Epub 2016 Jan 12.