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Exercise‐induced Calmodulin dependent protein kinase (CaMK)II activation regulates saturated and unsaturated fatty acids in rat skeletal muscle
Author(s) -
Mukwevho Emmanuel
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.883.5
Subject(s) - camk , medicine , palmitoleic acid , oleic acid , endocrinology , lauric acid , fatty acid , chemistry , skeletal muscle , metabolic syndrome , biochemistry , linoleic acid , obesity , protein kinase a , kinase , autophosphorylation
CaMKII regulates many pathways involved in the regulation of various cellular and molecular mechanisms that result in myriad health benefits. Exercise is a key activator of CaMKII, and shown to improve many functional activities in individuals who exercise compared with those who do not exercise, however the mechanism involved not yet fully elucidated. Fatty acids play crucial role in the pathogenesis of metabolic diseases such as type 2 diabetes, obesity, and metabolic syndromes (MetS) (Haffner et al. , 1992; Hanson et al. , 2002). Since fatty acid have been implicated in the aetiology of metabolic disease, exercise through its activation of CaMKII can prove to be a vital tool in finding therapeutic modalities for treating of the metabolic syndrome. Lipids were analysed from rats muscle using GC×GC TOFMS. Palmitoleic acid and oleic acid which are monounsaturated fatty acids known to promote insulin sensitivity and improve glycaemic control were investigated. Levels of the exercise group showed ~2.0 fold increase compared with the non‐exercise (control) group. Abolishing CaMKII activity by administration of KN93 significantly decreased exercise‐induced Palmitoleic acid levels. Oleic acid levels of the exercise group were ~ 4.1 folds higher than the non‐exercise group and followed the same pattern as Palmitoleic acid. Lauric acid is a saturated fatty acid, which increases fatty acid needed for better health. The exercise group showed ~ 8.7 fold increase compared with the non‐exercise group of Lauric acid. The exercise + KN93 group significantly reduced induction by ~2.5 fold compared with the exercise group. On the other hand, Myristic acid and palmitic acid which are saturated fatty acids known to increase risk factors of metabolic syndrome. The myristic acid level of the exercise group decreased by ~3.4 fold compared with the control group, whereas the exercise + KN93 group significantly increased by ~4.3 compared with the exercise group. In conclusion, this study shows that CaMKII activation by exercise regulates saturated and unsaturated fatty acids. Therefore, CaMKII can reduce the risk factors of metabolic syndrome and type 2 diabetes. Support or Funding Information National Research Foundation of South Africa