Abstract
Introduction: Metformin is a key treatment for type 2 diabetes, often linked to
oxidative stress and genetic factors like GSTM1 and GSTT1 variations.
Methods: We studied 150 subjects, examining how their deletion polymorphisms in these
genes correlate with Met treatment response. Those with GSTM1/T1 deletions (-/-) had a
higher T2DM risk (2.71-fold, P=0.005).
Results: Met responders with GSTM1(16bp) deletions had lower glucose levels compared
to non-responders (P<0.0001), and similar trends were observed with
GSTT1(54bp) deletions. Responders with both deletions also managed lipids better
(P=0.0256; P=0.0151). Non-responders with GSTM1/T1 null genotypes had better HDL
management (P=0.007).
Conclusion: These findings suggested that GSTM1 deletion could predict T2DM susceptibility
and Met response.
Keywords:
Glutathione S-transferase deletion polymorphism, pharmacogenetics, metformin-antidiabetic therapy (Met-ADT), prognostic biomarker, type 2 diabetes mellitus (T2DM), non-communicable diseases.
Graphical Abstract
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