PMID- 31328833
OWN - NLM
STAT- MEDLINE
DCOM- 20200807
LR  - 20210110
IS  - 1469-445X (Electronic)
IS  - 0958-0670 (Print)
IS  - 0958-0670 (Linking)
VI  - 104
IP  - 10
DP  - 2019 Oct
TI  - Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance 
      training-mediated myonuclear accretion and muscle mass gain in rats.
PG  - 1518-1531
LID - 10.1113/EP087585 [doi]
AB  - NEW FINDINGS: What is the central question of this study? Type 2 diabetes 
      mellitus (T2DM) causes skeletal muscle atrophy; does it affect resistance 
      training (RT)-mediated molecular adaptations and subsequent muscle hypertrophy? 
      What is the main finding and its importance? Although skeletal muscle mass and 
      regulation were not preserved under conditions of T2DM, the response of 
      RT-induced skeletal muscle hypertrophy was not impaired in T2DM rat skeletal 
      muscle. These findings suggest that the capacity of RT-mediated muscle mass gain 
      is not diminished in the T2DM condition. ABSTRACT: Type 2 diabetes mellitus 
      (T2DM) is known to cause skeletal muscle atrophy. However, it is not known 
      whether T2DM affects resistance training (RT)-mediated molecular adaptations and 
      subsequent muscle hypertrophy. Therefore, we investigated the effect of T2DM on 
      response of skeletal muscle hypertrophy to chronic RT using a rat resistance 
      exercise mimetic model. T2DM and healthy control rats were subjected to 18 bouts 
      (3 times per week) of chronic RT on unilateral lower legs. RT significantly 
      increased gastrocnemius muscle mass and myonuclei in both T2DM and healthy 
      control rats to the same extent, even though T2DM caused muscle atrophy in the 
      resting condition. Further, T2DM significantly reduced mechanistic target of 
      rapamycin complex 1 (mTORC1) activity (phosphorylation of p70S6K(Thr389) and 
      4E-BP1(Thr37/46) ) to insulin stimulation and the number of myonuclei in the 
      untrained basal condition, but RT-mediated adaptations were not affected by T2DM. 
      These findings suggested that although the skeletal muscle mass and regulation 
      were not preserved under basal conditions of T2DM, the response of RT-induced 
      skeletal muscle hypertrophy was not impaired in T2DM rat skeletal muscle.
CI  - (c) 2019 The Authors. Experimental Physiology Published by John Wiley & Sons Ltd on 
      behalf of The Physiological Society.
FAU - Ato, Satoru
AU  - Ato S
AD  - Graduate School of Sport and Health Science, Ritsumeikan University, Kusatsu, 
      Japan.
FAU - Kido, Kohei
AU  - Kido K
AD  - Graduate School of Sport and Health Science, Ritsumeikan University, Kusatsu, 
      Japan.
FAU - Sato, Koji
AU  - Sato K
AD  - Faculty of Human Development, Kobe University, Kobe, Japan.
FAU - Fujita, Satoshi
AU  - Fujita S
AUID- ORCID: 0000-0002-2297-1647
AD  - Graduate School of Sport and Health Science, Ritsumeikan University, Kusatsu, 
      Japan.
LA  - eng
GR  - 17H02183/Japan Society for the Promotion of Science/International
GR  - 14533567/Japanese Council for Science, Technology and Innovation/International
GR  - NARO/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190813
PL  - England
TA  - Exp Physiol
JT  - Experimental physiology
JID - 9002940
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
SB  - IM
MH  - Adaptation, Physiological
MH  - Adipose Tissue/growth & development
MH  - Animals
MH  - Cell Nucleus/pathology
MH  - Diabetes Mellitus, Type 2/complications/*pathology
MH  - Hypoglycemic Agents/pharmacology
MH  - Insulin/pharmacology
MH  - Male
MH  - Mechanistic Target of Rapamycin Complex 1/metabolism
MH  - Muscle Fibers, Skeletal
MH  - Muscle, Skeletal/*growth & development/*pathology
MH  - Muscular Atrophy/etiology/*pathology
MH  - Organ Size
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Inbred OLETF
MH  - *Resistance Training
PMC - PMC6790689
OTO - NOTNLM
OT  - muscle hypertrophy
OT  - resistance training
OT  - type 2 diabetes
COIS- All authors declare no conflict of interest.
EDAT- 2019/07/23 06:00
MHDA- 2020/08/08 06:00
PMCR- 2019/10/14
CRDT- 2019/07/23 06:00
PHST- 2019/01/12 00:00 [received]
PHST- 2019/07/19 00:00 [accepted]
PHST- 2019/07/23 06:00 [pubmed]
PHST- 2020/08/08 06:00 [medline]
PHST- 2019/07/23 06:00 [entrez]
PHST- 2019/10/14 00:00 [pmc-release]
AID - EPH12566 [pii]
AID - 10.1113/EP087585 [doi]
PST - ppublish
SO  - Exp Physiol. 2019 Oct;104(10):1518-1531. doi: 10.1113/EP087585. Epub 2019 Aug 13.