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The majority of Mexican patients with diabetes mellitus type 2 (DMT2) (67.9-85.0%) are prescribed sulphonylureas (SUs), which are metabolized by cytochrome P450 2C9 (abbreviated as CYP2C9 ). SUs are a type of oral anti-diabetic compound which inhibit ATP-sensitive potassium channels, thus inducing glucose-independent insulin release by the β-pancreatic cells. The wide variability reported in SU responses has been attributed to the polymorphisms of CYP2C9 . The present study aimed to describe CYP2C9 polymorphisms (*2 , *3 and IVS8-109T ) within a sample of Mexican patients with DMT2, while suggesting the potential clinical implications in terms of glibenclamide response variability. From a sample of 248 patients with DMT2 who initially consented to be studied, those ultimately included in the study were treated with glibenclamide (n=11), glibenclamide combined with metformin (n=112) or metformin (n=76), and were subsequently genotyped using a reverse transcription-quantitative polymerase chain reaction (PCR), end-point allelic discrimination and PCR amplifying enzymatic restriction fragment long polymorphism. Clinical data were gathered through medical record revision. The frequencies revealed were as follows: CYP2C9*1 / *1 , 87.5%; *1 / *2 , 6.5%; *1 / *3 , 5.2%; and CYP2C9 , IVS8-109A&gt;T , 16.1%. Glibenclamide significantly reduced the level of pre-prandial glucose (P&lt;0.01) and the percentage of glycated hemoglobin (%HbA1c; P&lt;0.01) for IVS8-109A&gt;T compared with combined glibenclamide and metformin treatment. Concerning the various treatments with respect to the different genotypes, the percentages obtained were as follows: Glibenclamide A / A , HbA1c&lt;6.5=33.3%; glibenclamide + metformin A / A , HbA1c&lt;6.5=24.6%; glibenclamide A / T , HbA1c&lt;6.5=33.3%; glibenclamide + metformin A / T , HbA1c&lt;6.5=25%; glibenclamide T / T , HbA1c&lt;6.5=100%; and glibenclamide + metformin T / T , HbA1c&lt;6.5=12.5%. Altogether, these results revealed that, although genetically customized prescriptions remain a desirable goal to increase the chances of therapeutic success, within the studied population neither allelic variants nor dosages demonstrated a clear association with biomarker levels. A key limitation of the present study was the lack of ability to quantify either the plasma concentrations of SU or their metabolites; therefore, further, precise experimental and observational studies are required.

biomedical reports

Frequency of CYP2C9 (*2, *3 and IVS8‑109A&gt;T) allelic variants, and their clinical implications, among Mexican patients with diabetes mellitus type 2 undergoing treatment with glibenclamide and metformin