obesity-2016_posters-accepted-abstracts

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Volume 6, Issue 9(Suppl) J Obes Weight Loss Ther 2016
ISSN: 2165-7904 JOWT, an open access journal
Page 59
Obesity 2016
December 08-10, 2016
conferenceseries.com
Obesity & Weight Management
December 08-10, 2016 Dallas, USA
10th International Conference and Exhibition on
J Obes Weight Loss Ther 2016, 6:9(Suppl)
Calmodulin dependent protein kinase (CaMK)-II activation by exercise regulates lipid metabolism in rat
skeletal muscle
Sandile Lawrence Fuku
North-West University, South Africa
Background: Activation of calmodulin dependent protein kinase (CaMK)-II by exercise has plethora of benefits in metabolism and
health. Regulation of lipid metabolism is very significant to alleviate type-2 diabetes and obesity. The role of CaMKII in the regulation
of genes that are involved in lipid metabolism has not been studied yet, which became the focus of this study.
Methods: 5-6 weeks old male Wistar rats were used in this study. Western blot was performed to assess the protein expression of
Carnitine palmitoyltransferase (CPT)-1 and Acetyl-CoA carboxylase (ACC)-1. Cpt-1 and Acc-1 gene expressions were assessed
using Quantitative real time PCR (qPCR).
Results: The results indicate that exercise-induced CaMKII activation increases CPT-1 expression and decreases ACC-1 expression
in rat skeletal muscle. Thus, confirming CaMKII activation by exercise and the resultant increase in lipid oxidation. Administration
of KN93 (CaMKII inhibitor) reversed all exercise-induced changes.
Conclusions: This study demonstrated that CaMKII activation, by exercise, regulates lipid metabolism genes in rat skeletal muscle.
Further, the increase in lipid oxidation and decrease in lipid synthesis are evidence of the regulatory role CaMKII in lipid metabolism.
CaMKII is a potential target in designing novel therapeutic drugs in the management and treatment of type-2 diabetes and obesity.