Incidence of new onset of type‑2 diabetes with the use of atenolol for treatment of hypertension in north indian population: No role of irs‑1 and kir 6.2 Gene polymorphism

Abstract

Introduction: Previous research has suggested that β1
adreno‑receptor blockers
commonly used for management of hypertension may promote new onset of type‑2
diabetes mellitus. The objective of this study is to evaluate the role of insulin receptor
substrate‑1 (IRS‑1) gene and pancreatic ATP‑sensitive potassium inward rectifying
channel (Kir 6.2) genetic polymorphism in induction of diabetes mellitus with chronic
use of β1
blocker. Materials and Methods: A total of 150 patients with essential
hypertension aged between 17 and 65 years who were diagnosed with essential
hypertension and prescribed atenolol therapy, were recruited. Of these, only
100 patients responding to atenolol were followed‑up for 12 months for monitoring
blood glucose level every month. The IRS‑1 and pancreatic ATP‑sensitive potassium
channel Kir 6.2 (E23K) gene polymorphism were genotyped using genomic DNA
extracted from the whole blood of the recruited patients by polymerase chain reaction
and restriction fragment length polymorphism. Results: This study revealed that
among the 100 patients responding to atenolol 27% showed a significant increase
in the fasting blood sugar. Genotyping study of the recruited patients revealed a
difference in allelic frequencies for IRS‑1 (Gly972Arg) and pancreatic ATP‑sensitive
potassium channel Kir 6.2 (E23K) variants. However, allelic distribution between
the hypertensive patients on atenolol showing hyperglycemia and normoglycemia was
not significantly different for these genes. Conclusion: Thus, showing no correlation,
for incidence of diabetes post atenolol therapy in the studied population with these
gene polymorphisms.