RESEARCH ARTICLE


Gene Expression of GSK3 in Type II Diabetics Compared to Non-Diabetics (ex vivo)



Somayeh A.H. Khorami1, Mohd S. Abd Mutalib1, Mohammad F. Shiraz2, Joseph A. Abdullah3, Zulida Rejali4, Razana M. Ali5, Huzwah Khaza’ai6, *
1 Department of Nutrition and Dietetic, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia
2 Department of Artificial Intelligence and Computer Engineering, Faculty of Electrical Engineering, Computer and IT, Qazvin Branch, Islamic Azad University, Qazvin, Iran
3 Perak Community Hospital, Ipoh, Malaysia
4 Department of Obstetrics and Gynaecology, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia
5 Department of Pathology, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia
6 Department of Biomedical Science, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia


© 2020 Khorami et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at Department of Biomedical Science, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia; E-mail: huzwah@upm.edu.my


Abstract

Background:

GSK3 is a serine/threonine kinase that is involved in the storage of glucose into glycogen through the negative regulation of glycogen synthase. Defects in GSK3 and glycogen synthase function are early stages of the development of insulin resistance, which may cause impaired glycogen synthesis in Type II diabetes.

Methods:

In this cross-sectional study, the gene expression level of GSK3 from Type II diabetic and non-diabetic participants was compared via real-time RT-PCR. To investigate the relationships between GSK3 expression and indicators of insulin resistance, Pearson's correlation analysis was performed. To compare the differences between GSK3 expression levels based on BMI categories, one-way ANOVA was used.

Results:

Gene expression of GSK3 was slightly higher in diabetic participants compared to non-diabetics, but it was statistically insignificant. Also, no significant difference was found based on BMI categories in the two groups. No significant association between GSK3 expression and indicators of insulin resistance was observed in non-diabetic participants. There was only a positive significant correlation between GSK3 expression and FBS in diabetic participants.

Conclusion:

These results indicate that the regulation of GSK3 may occur at the translation level, as gene expression level was unaltered between diabetic and non-diabetic participants. Also, since circulating levels of both glucose and insulin regulate GSK3 activity, tissue specificity for the expression and post-translation regulations of GSK3 may exist, which cause hyperactivation or overexpression in some target tissues in diabetes. Furthermore, it is probable that glycogen synthase activity is also regulated by non-insulin mediated mechanisms like exercise or allosteric changes, independent of GSK3 expression.

Keywords: GSK3, Gene expression, Type II diabetes, Insulin action, Metabolism, RT-PCR, Transcription.