PMID- 22938510
OWN - NLM
STAT- MEDLINE
DCOM- 20140124
LR  - 20211021
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 19
IP  - 3
DP  - 2013 Jul 20
TI  - Mitochondrial plasticity in obesity and diabetes mellitus.
PG  - 258-68
LID - 10.1089/ars.2012.4910 [doi]
AB  - SIGNIFICANCE: Insulin resistance and its related diseases, obesity and type 2 
      diabetes mellitus (T2DM), have been linked to changes in aerobic metabolism, 
      pointing to a possible role of mitochondria in the development of insulin 
      resistance. RECENT ADVANCES: Refined methodology of ex vivo high-resolution 
      respirometry and in vivo magnetic resonance spectroscopy now allows describing 
      several features of mitochondria in humans. In addition to measuring 
      mitochondrial function at baseline and after exercise-induced submaximal energy 
      depletion, the response of mitochondria to endocrine and metabolic challenges, 
      termed mitochondrial plasticity, can be assessed using hyperinsulinemic clamp 
      tests. While insulin resistant states do not uniformly relate to baseline and 
      post-exercise mitochondrial function, mitochondrial plasticity is typically 
      impaired in insulin resistant relatives of T2DM, in overt T2DM and even in type 1 
      diabetes mellitus (T1DM). CRITICAL ISSUES: The variability of baseline 
      mitochondrial function in the main target tissue of insulin action, skeletal 
      muscle and liver, may be attributed to inherited and acquired changes in either 
      mitochondrial quantity or quality. In addition to certain gene polymorphisms and 
      aging, circulating glucose and lipid concentrations correlate with both 
      mitochondrial function and plasticity. FUTURE DIRECTIONS: Despite the 
      associations between features of mitochondrial function and insulin sensitivity, 
      the question of a causal relationship between compromised mitochondrial 
      plasticity and insulin resistance in the development of obesity and T2DM remains 
      to be resolved.
FAU - Jelenik, Tomas
AU  - Jelenik T
AD  - Institute for Clinical Diabetology, German Diabetes Center, D-40225 Dusseldorf, 
      Germany.
FAU - Roden, Michael
AU  - Roden M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20121009
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Diabetes Mellitus, Type 2/*metabolism
MH  - Glucose/metabolism
MH  - Humans
MH  - Insulin Resistance
MH  - Lipid Metabolism
MH  - Mitochondria/*metabolism
MH  - Obesity/*metabolism
PMC - PMC3691915
EDAT- 2012/09/04 06:00
MHDA- 2014/01/25 06:00
PMCR- 2014/07/20
CRDT- 2012/09/04 06:00
PHST- 2012/09/04 06:00 [entrez]
PHST- 2012/09/04 06:00 [pubmed]
PHST- 2014/01/25 06:00 [medline]
PHST- 2014/07/20 00:00 [pmc-release]
AID - 10.1089/ars.2012.4910 [pii]
AID - 10.1089/ars.2012.4910 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2013 Jul 20;19(3):258-68. doi: 10.1089/ars.2012.4910. Epub 
      2012 Oct 9.