Biography

Biography: Emmanuel Mukewevho

Abstract

CaMKII regulates many pathways involved in the regulation of various cellular and molecular mechanisms that result\r\nin myriad health benefits. Exercise is a key activator of CaMKII, and shown to improve many functional activities in\r\nindividuals who exercise compared with those who do not exercise, however the mechanism involved not yet fully elucidated,\r\nwhich became the objective of this study.\r\nIn this study using rats, we investigated various lipids metabolism for both saturated and non-saturated fatty acids in\r\nrats that exercised, non-exercised and exercised+KN93 (CaMKII inhibitor). Lipids were analysed using GC×GC TOFMS.\r\nPalmitoleic acid and oleic acid which are monounsaturated fatty acids known to promote insulin sensitivity and improve\r\nglycaemic control were investigated. Levels of the exercise group showed ~2.0 fold increase compared with the non-exercise\r\n(control) group. Abolishing CaMKII activity by administration of KN93 significantly decreased exercise-induced Palmitoleic\r\nacid levels. Oleic acid levels of the exercise group were ~ 4.1 folds higher than the non-exercise group and followed the same\r\npattern as Palmitoleic acid.\r\nLauric acid is a saturated fatty acid, which increases fatty acid needed for better health. The exercise group showed ~ 8.7\r\nfold increase compared with the non-exercise group of Lauric acid. The exercise + KN93 group significantly reduced induction\r\nby ~2.5 fold compared with the exercise group. On the other hand, Myristic acid and palmitic acid which are saturated fatty\r\nacids known to increase risk factors of metabolic syndrome. The myristic acid level of the exercise group decreased by ~3.4\r\nfold compared with the control group, whereas the exercise + KN93 group significantly increased by ~4.3 compared with the\r\nexercise group.\r\nIn conclusion, CaMKII can reduce the risk factors of metabolic syndrome and type 2 diabetes.