PMID- 26057538
OWN - NLM
STAT- MEDLINE
DCOM- 20160425
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 6
DP  - 2015
TI  - Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in 
      Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo.
PG  - e0129579
LID - 10.1371/journal.pone.0129579 [doi]
LID - e0129579
AB  - Insulin resistance, altered lipid metabolism and mitochondrial dysfunction in 
      skeletal muscle would play a major role in type 2 diabetes mellitus (T2DM) 
      development, but the causal relationships between these events remain 
      conflicting. To clarify this issue, gastrocnemius muscle function and energetics 
      were investigated throughout a multidisciplinary approach combining in vivo and 
      in vitro measurements in Goto-Kakizaki (GK) rats, a non-obese T2DM model 
      developing peripheral insulin resistant without abnormal level of plasma 
      non-esterified fatty acids (NEFA). Wistar rats were used as controls. Mechanical 
      performance and energy metabolism were assessed strictly non-invasively using 
      magnetic resonance (MR) imaging and 31-phosphorus MR spectroscopy (31P-MRS). 
      Compared with control group, plasma insulin and glucose were respectively lower 
      and higher in GK rats, but plasma NEFA level was normal. In resting GK muscle, 
      phosphocreatine content was reduced whereas glucose content and intracellular pH 
      were both higher. However, there were not differences between both groups for 
      basal oxidative ATP synthesis rate, citrate synthase activity, and 
      intramyocellular contents for lipids, glycogen, ATP and ADP (an important in vivo 
      mitochondrial regulator). During a standardized fatiguing protocol (6 min of 
      maximal repeated isometric contractions electrically induced at a frequency of 
      1.7 Hz), mechanical performance and glycolytic ATP production rate were reduced 
      in diabetic animals whereas oxidative ATP production rate, maximal mitochondrial 
      capacity and ATP cost of contraction were not changed. These findings provide in 
      vivo evidence that insulin resistance is not caused by an impairment of 
      mitochondrial function in this diabetic model.
FAU - Macia, Michael
AU  - Macia M
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Pecchi, Emilie
AU  - Pecchi E
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Vilmen, Christophe
AU  - Vilmen C
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Desrois, Martine
AU  - Desrois M
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Lan, Carole
AU  - Lan C
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Portha, Bernard
AU  - Portha B
AD  - Universitx Paris-Diderot, Sorbonne Paris Cite, Laboratoire B2PE, Unite BFA, CNRS 
      EAC 4413, Paris, France.
FAU - Bernard, Monique
AU  - Bernard M
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Bendahan, David
AU  - Bendahan D
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
FAU - Giannesini, Benoit
AU  - Giannesini B
AD  - Aix-Marseille Universite, CNRS, CRMBM UMR 7339, 13385, Marseille, France.
LA  - eng
PT  - Journal Article
DEP - 20150609
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 020IUV4N33 (Phosphocreatine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Diabetes Mellitus, Experimental/metabolism/*pathology/*physiopathology
MH  - Electric Stimulation
MH  - Energy Metabolism
MH  - Hydrogen-Ion Concentration
MH  - *Insulin Resistance
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Mitochondria/*metabolism
MH  - *Muscle Contraction
MH  - Muscle, Skeletal/metabolism/pathology/*physiopathology
MH  - Phosphocreatine/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Time Factors
PMC - PMC4461248
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/06/10 06:00
MHDA- 2016/04/26 06:00
PMCR- 2015/06/09
CRDT- 2015/06/10 06:00
PHST- 2015/01/28 00:00 [received]
PHST- 2015/05/11 00:00 [accepted]
PHST- 2015/06/10 06:00 [entrez]
PHST- 2015/06/10 06:00 [pubmed]
PHST- 2016/04/26 06:00 [medline]
PHST- 2015/06/09 00:00 [pmc-release]
AID - PONE-D-15-04137 [pii]
AID - 10.1371/journal.pone.0129579 [doi]
PST - epublish
SO  - PLoS One. 2015 Jun 9;10(6):e0129579. doi: 10.1371/journal.pone.0129579. 
      eCollection 2015.