Calmodulin dependent protein kinase II activation by exercise regulates saturated & unsaturated fatty acids and improves some metabolic syndrome markers
- PMID: 25046734
- DOI: 10.1016/j.lfs.2014.07.013
Calmodulin dependent protein kinase II activation by exercise regulates saturated & unsaturated fatty acids and improves some metabolic syndrome markers
Abstract
Aims: Activation of Calmodulin dependent protein kinase (CaMK)-II by exercise has a plethora of benefits in health. Fatty acids play a pivotal role in the pathogenesis of metabolic syndrome (MetS). Prevention of MetS and treatment of its main characteristics are very significant to fight against type 2 diabetes. CaMKII activation in the regulation of saturated and unsaturated fatty acids in relation to type 2 diabetes and MetS has not been studied, which became the focus of this present study.
Main methods: Using Gas chromatography-Mass spectrometry, we investigated saturated fatty acids and unsaturated fatty acids. Quantitative real time PCR was also used to assess the gene expression.
Key findings: Results indicate that both palmitoleic acid and oleic acid which are monounsaturated fatty acids were increased in response to CaMKII activation. On the other hand, myristic acid and palmitic acid which are saturated fatty acids known to increase the risk factors of MetS and type 2 diabetes were decreased by exercise induction of CaMKII. Conversely, lauric acid also a saturated fatty acid was increased in response to CaMKII activation by exercise. This fatty acid is known to have beneficial effects in alleviating symptoms of both type 2 diabetes and MetS.
Significance: According to our knowledge, this is the first study to show that CaMKII activation by exercise regulates fatty acids essential in type 2 diabetes and MetS. CaMKII can be an avenue of designing novel therapeutic drugs in the management and treatment of type 2 diabetes and MetS.
Keywords: CaMKII; Exercise; MetS; Saturated fatty acids; Type 2 diabetes; Unsaturated fatty acids.
Copyright © 2014 Elsevier Inc. All rights reserved.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical