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Int. J. Mol. Sci. 2009, 10(1), 306-324; doi:10.3390/ijms10010306
Review
Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences
1
INRA, UMR1019 Nutrition Humaine, F-63120 Saint Genès Champanelle, France
2
Université Clermont 1, UFR Médecine, UMR1019 Nutrition Humaine, F-63000 Clermont-Ferrand, France
* Author to whom correspondence should be addressed.
Received: 10 October 2008; in revised form: 7 January 2009 / Accepted: 9 January 2009 / Published: 13 January 2009
(This article belongs to the Special Issue Molecular System Bioenergetics)
Abstract: Mitochondria play a key role in the energy metabolism in skeletal muscle. A new concept has emerged suggesting that impaired mitochondrial oxidative capacity in skeletal muscle may be the underlying defect that causes insulin resistance. According to current knowledge, the causes and the underlying molecular mechanisms at the origin of decreased mitochondrial oxidative capacity in skeletal muscle still remain to be elucidated. The present review focuses on recent data investigating these issues in the area of metabolic disorders and describes the potential causes, mechanisms and consequences of mitochondrial dysfunction in the skeletal muscle.
Keywords: Mitochondrial dysfunction; skeletal muscle; metabolic disorders; obesity; insulin resistance; type 2 diabetes
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MDPI and ACS Style
Chanséaume, E.; Morio, B. Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences. Int. J. Mol. Sci. 2009, 10, 306-324.
AMA StyleChanséaume E, Morio B. Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences. International Journal of Molecular Sciences. 2009; 10(1):306-324.
Chicago/Turabian StyleChanséaume, Emilie; Morio, Béatrice. 2009. "Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences." Int. J. Mol. Sci. 10, no. 1: 306-324.
Int. J. Mol. Sci.
EISSN 1422-0067
Published by MDPI AG, Basel, Switzerland
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