Exercise, CaMKII, and type 2 diabetes

Authors

  • Jitcy S. Joseph Department of Toxicology and Biochemistry, National Institute for Occupational Health, A division of National Health Laboratory Service, Johannesburg, South Africa, Phone +27 832902722, E-mail: jitcysaji@gmail.com; jitcyj@nioh.ac.za https://orcid.org/0000-0001-9113-989X
  • Krishnan Anand Department of Chemical Pathology, School of Pathology, Faculty of Health Sciences and National Health Laboratory Service, University of the Free State, Bloemfontein, South Africa
  • Sibusiso T. Malindisa Department of Life and Consumer Sciences, University of South Africa (UNISA), Florida Park, Johannesburg, South Africa https://orcid.org/0000-0002-9287-9408
  • Adewale O. Oladipo Institute for Nanotechnology and Water Sustainability (iNanoWS), College of Science, Engineering and Technology, University of South Africa, Science Park Florida, Johannesburg, 1710, South Africa https://orcid.org/0000-0002-3454-5768
  • Oladapo F. Fagbohun Department of Biomedical Engineering, First Technical University, Ibadan, Oyo State, Nigeria; Department of Pediatrics, Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB, Canada https://orcid.org/0000-0002-1340-6697

DOI:

https://doi.org/10.17179/excli2020-3317

Keywords:

exercise, type 2 diabetes, CaMKII, GLUT4, mitochondrial biogenesis, insulin resistance

Abstract

Individuals who exercise regularly are protected from type 2 diabetes and other metabolic syndromes, in part by enhanced gene transcription and induction of many signaling pathways crucial in correcting impaired metabolic pathways associated with a sedentary lifestyle. Exercise activates Calmodulin-dependent protein kinase (CaMK)II, resulting in increased mitochondrial oxidative capacity and glucose transport. CaMKII regulates many health beneficial cellular functions in individuals who exercise compared with those who do not exercise. The role of exercise in the regulation of carbohydrate, lipid metabolism, and insulin signaling pathways are explained at the onset. Followed by the role of exercise in the regulation of glucose transporter (GLUT)4 expression and mitochondrial biogenesis are explained. Next, the main functions of Calmodulin-dependent protein kinase and the mechanism to activate it are illustrated, finally, an overview of the role of CaMKII in regulating GLUT4 expression, mitochondrial biogenesis, and histone modification are discussed.

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Published

2021-02-17

How to Cite

Joseph, J. S., Anand, K. ., Malindisa, S. T., Oladipo, A. O., & Fagbohun, O. F. (2021). Exercise, CaMKII, and type 2 diabetes. EXCLI Journal, 20, 386–399. https://doi.org/10.17179/excli2020-3317

Issue

Vol. 20 (2021)

Section

Review articles

License

Copyright (c) 2021 Jitcy S. Joseph, Krishnan Anand, Sibusiso T. Malindisa, Adewale O. Oladipo, Oladapo F. Fagbohun

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