1. Department of Health Risk Management, China Medical University, 40402 Taichung, Taiwan;
2. Department of Anatomical Pathology, Taipei Institute of Pathology, School of Medicine, National Yang-Ming University , 11221 Taipei, Taiwan;
3. Division of Plastic and Reconstructive Surgery, China Medical University Hospital, 40402 Taichung, Taiwan;
4. School of Chinese Medicine, China Medical University, 40402 Taichung, Taiwan;
5. Genetics Center, Medical Research, China Medical University Hospital, 40447 Taichung, Taiwan;
6. Department of Medical Genetics, China Medical University Hospital, 40447 Taichung, Taiwan, R.O.C.
# YCL and YHW contributed equally to this work and are co-first authors to this article.
Diabetes mellitus (DM) is a chronic disease found worldwide. Notably, BKS.Cg- Dock7m +/+ Leprdb/JNarl mice are useful animal models for studying type 2 diabetes mellitus (T2DM). In this study, we investigated casein kinase 2 alpha 1 (CSNK2A1) gene and protein expression in the liver tissues of mice at different ages (4, 16, and 32 weeks) using real-time quantitative polymerase chain reactions, western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay. Our data paved the way for exploring BKS.Cg- Dock7m +/+ Leprdb/JNarl in the mouse model by demonstrating a significant increase in gene and protein expression in T2DM (+Leprdb/+Leprdb) mouse liver when compared to control (+Dock7m/+Dock7m) mouse liver. We also observed that CSNK2A1 protein level in the serum of T2DM patient group was higher than that of the control group, although the data was not statistically significant. Based on our findings, we can now understand the role of CSNK2A1 gene upregulation when encountering T2DM pathologies.
Keywords: +Leprdb / +Leprdb mice, T2DM, Casein Kinase 2 Alpha 1 (CSNK2A1).