Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes
AbstractSkeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation and accumulation of fatty acid intermediates in the form of long and medium chain acylcarnitines, may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity. The present review discusses the roles of anterograde and retrograde communication in nucleo-mitochondrial crosstalk that determines skeletal muscle mitochondrial adaptations, specifically alterations in mitochondrial number and function in relation to obesity and insulin resistance. Special emphasis is placed on the effects of high fat diet (HFD) feeding on expression of nuclear-encoded mitochondrial genes (NEMGs) nuclear receptor factor 1 (NRF-1) and 2 (NRF-2) and peroxisome proliferator receptor gamma coactivator 1 alpha (PGC-1α) in the onset and progression of insulin resistance during obesity and how HFD-induced alterations in NEMG expression affect skeletal muscle mitochondrial adaptations in relation to beta oxidation of fatty acids. Finally, the potential ability of acylcarnitines or fatty acid intermediates resulting from mitochondrial beta oxidation to act as retrograde signals in nucleo-mitochondrial crosstalk is reviewed and discussed. View Full-Text
Share & Cite This Article
Devarshi, P.P.; McNabney, S.M.; Henagan, T.M. Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes. Int. J. Mol. Sci. 2017, 18, 831.
Devarshi PP, McNabney SM, Henagan TM. Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes. International Journal of Molecular Sciences. 2017; 18(4):831.Chicago/Turabian Style
Devarshi, Prasad P.; McNabney, Sean M.; Henagan, Tara M. 2017. "Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes." Int. J. Mol. Sci. 18, no. 4: 831.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.