Pharmacogenomic association between a variant in SLC47A1 gene and therapeutic response to metformin in type 2 diabetes

Pharmacogenetic studies revealed that variants in genes related to the pharmacokinetics of metformin were associated with glucose‐lowering effect of metformin. The aim of this study was to investigate possible associations of the variants in genes encoding organic cationic transporters–solute carrie...

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Published in:Diabetes, obesity & metabolism obesity & metabolism, 2013-02, Vol.15 (2), p.189-191
Main Authors: Tkáč, I., Klimčáková, L., Javorský, M., Fabianová, M., Schroner, Z., Hermanová, H., Babjaková, E., Tkáčová, R.
Format: Article
Language:English
Subjects:
Alleles
Diabetes Mellitus, Type 2 - drug therapy
Diabetes Mellitus, Type 2 - genetics
Dose-Response Relationship, Drug
Double-Blind Method
Female
Genotype
glycaemic control
Humans
Hypoglycemic Agents - pharmacology
Male
metformin
Metformin - pharmacology
Middle Aged
Organic Cation Transport Proteins
pharmacogenetics
Polymorphism, Single Nucleotide
Treatment Outcome
type 2 diabetes
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Summary:Pharmacogenetic studies revealed that variants in genes related to the pharmacokinetics of metformin were associated with glucose‐lowering effect of metformin. The aim of this study was to investigate possible associations of the variants in genes encoding organic cationic transporters–solute carrier family 22, members A1, A2 (SLC22A1, SLC22A2) and solute carrier family 47, member A1 (SLC47A1) with response to metformin in type 2 diabetes. One hundred forty‐eight drug‐naive patients with type 2 diabetes were included in the study. Genotyping for SLC22A1 rs622342, SLC22A2 rs316019 and SLC47A1 rs2289669 variants was performed using real‐time PCR with subsequent melting‐curve analysis. SLC47A1 rs2289669 genotype was significantly associated with the reduction in haemoglobin A1c (HbA1c) after 6 months. Twenty percentage of patients with diabetes that are homozygous for A‐allele of SLC47A1 had twofold reduction in HbA1c in comparison with the patients carrying G‐allele (GG + GA: 0.55 ± 0.09% vs. AA: 1.10 ± 0.18%, p = 0.018). In conclusion, the results of this study might have in future practical implication in personalised treatment of patients with type 2 diabetes.
ISSN:1462-8902
1463-1326
DOI:10.1111/j.1463-1326.2012.01691.x