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ORIGINAL ARTICLE
Year : 2014  |  Volume : 5  |  Issue : 1  |  Page : 50-55

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


1 Department of Pharmacology, Seth G.L. Bihani S.D College of Technical Education, Sri Ganganagar, Rajasthan, India
2 Department of Biotechnology, Punjabi University, Patiala, Punjab, India
3 Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India

Correspondence Address:
Rajesh K Goel
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala 147 002
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0976-9234.136797

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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.


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