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Volume 6, Issue 9(Suppl) J Obes Weight Loss Ther 2016
ISSN: 2165-7904 JOWT, an open access journal Obesity 2016
December 08-10, 2016
Page 43
Notes:
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Obesity & Weight Management
December 08-10, 2016 Dallas, USA
10th International Conference and Exhibition on
Calmodulin dependent protein kinase (CaMK)II activation by exercise regulates NRF-1 and its target
lipid oxidizing target gene, Cpt-1 in rat skeletal muscle
Regular exercise increases oxidation of fatty acids in skeletal muscle. Exercise activates Calmodulin-dependent protein
kinase (CaMK)II, resulting in increased mitochondrial oxidative capacity. As such, exercise can curb accumulation
of excess lipids in adipose and intramuscular tissues that may result in obesity/type 2 diabetes. Lipid metabolism mainly
occurs in mitochondria regulated by NRF-1 and is controlled by a set of mitochondrial enzymes. For example, Carnitine
palmitoyltransferase (CPT)-1 is a rate-limiting enzyme in mitochondrial lipid oxidation that regulates the transport of long
chain fatty acids across the mitochondrial membrane, resulting in ATP synthesis. On the other hand, acetyl-CoA carboxylase
(ACC)-1 is a mitochondrial enzyme that promotes lipid synthesis by providing malonyl CoA substrate for the biosynthesis of
fatty acids. NRF-1 is the major transcriptional factor of the mitochondria, the site for ATP generation from carbohydrates and
lipids. As such, mitochondrial dysfunction is crucial in metabolism of the cell. In order to investigate the amount of NRF-1
bound Cpt-1, ChIP assay performed. Exercise showed that the amount of NRF-1 bound Cpt-1 was ~1.3 fold increase compared
with the control group. The exercise + KN93 group did not show any significant change compared with the exercise group.
This result indicates that exercise-induced CaMKII activation increase the amount of NRF-1 bound Cpt-1. With respective to
gene transcription, exercise group showed ~7.8 fold increase compared with the control group. Cpt-1 gene expression of the
exercise + KN93 group showed significant decrease compared with the exercise group. Cpt-1 gene expression of the exercise +
KN93 was similar to the control group. This result shows that CaMKII activation increase Cpt-1 gene expression in rat skeletal
muscle. With respect to mitochondrial integrity, mitochondria size of the exercise group increased by ~3.0 fold compared with
the control group, whereas the exercise + KN93 group showed significant decrease compared with the exercise group. Using
TEM we show that exercise-induced CaMKII activation increases mitochondria size in rat skeletal muscle and its integrity.
Biography
Emmanuel Mukwevho has completed his PhD in 2010 from University of Cape Town, South Africa in Anatomy and Cell Biology. He is an Associate Professor of
Biochemistry at North West University, South Africa. He has published both nationally and internationally in reputed journals and his specialty is in Obesity and
Diabetes where he led the Diabetes & Obesity Therapeutics Research group at North West University.
Emmanuel Mukwevho
North West University, South Africa
Emmanuel Mukwevho, J Obes Weight Loss Ther 2016, 6:9(Suppl)