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>T
, 16.1%. Glibenclamide significantly reduced the level of pre-prandial glucose (P<0.01) and the percentage of glycated hemoglobin (%HbA1c; P<0.01) for
IVS8-109A>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<6.5=33.3%; glibenclamide + metformin
A
/
A
, HbA1c<6.5=24.6%; glibenclamide
A
/
T
, HbA1c<6.5=33.3%; glibenclamide + metformin
A
/
T
, HbA1c<6.5=25%; glibenclamide
T
/
T
, HbA1c<6.5=100%; and glibenclamide + metformin
T
/
T
, HbA1c<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.