Research Article

Effects of the drugs gliclazide and metformin on solute carrier family 2 member 2 (SLC2A2) gene expression in type 2 diabetic patients in Vietnam

Published: March 14, 2023
Genet. Mol. Res. 22(1): GMR19054 DOI: https://doi.org/10.4238/gmr19054
Cite this Article:
D.M. Nguyen, M.T. Nguyen, T.T.Bich Vo, M.N. Nghiem, S.T. Dao (2023). Effects of the drugs gliclazide and metformin on solute carrier family 2 member 2 (SLC2A2) gene expression in type 2 diabetic patients in Vietnam. Genet. Mol. Res. 22(1): GMR19054. https://doi.org/10.4238/gmr19054
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Abstract

In recent years, the number of people with type 2 diabetes mellitus has increased rapidly and it has become an important public health problem in Vietnam. To provide valuable information on the efficacy and safety of diabetes medications (metformin and gliclazide), we evaluated how they affected the expression level and mutations of the SLC2A2 gene in the liver of T2DM patients. The SLC2A2 gene was analyzed in 165 patients with T2DM and 54 control subjects. Anthropometry, clinical parameters, molecular analysis, and gene expression were examined. We discovered high levels of mRNA SLC2A2 expression in the livers of people with T2DM who did not receive drug treatment. These levels were 1.5 times higher when compared to other groups that received drug treatment. Mutations of the SLC2A2 gene sequence were recorded in two T2DM patients belonging to the therapy group (c.1127T>G (p.Met376Arg) in exon 9 and c.609T>C (p.Ser203Ser) in exon 5). Finally, we found a strong and significant relationship between the glycemic control index and two enzymes, alanine aminotransferase and aspartate aminotransferase, with mRNA SLC2A2 expression under therapy. Our findings identified mutations of the SLC2A2 gene and a positive correlation between SLC2A2 gene expression and the effects of gliclazide and metformin in the liver of T2DM patients. This might contribute to a better understanding of the SLC2A2 gene, and the safety and tolerability of metformin and gliclazide therapy.

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