Genetic variants identified from GWAS for predisposition to type 2 diabetes predict sulfonylurea drug response

N. M. Phani; M. Vohra; P. Adhikari; S. K. Nagri; U. Shashikiran; S. C. D’Souza; P. R.R. Kalluri; K. Satyamoorthy; P. S. Rai

doi:10.2174/1566524018666180222122653

Genetic variants identified from GWAS for predisposition to type 2 diabetes predict sulfonylurea drug response

N. M. Phani
, M. Vohra
, P. Adhikari
, S. K. Nagri
, U. Shashikiran
, S. C. D’Souza
, P. R.R. Kalluri
, K. Satyamoorthy
, P. S. Rai^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

Background: Several SNPs were identified through GWAS for their association with type 2 diabetes which has implications to pancreatic β-cell physiology. Objective: We aimed to study the role of risk alleles of TCF7L2, KCNJ11, CDKN2A, CDKAL1, IGF2BP2, SLC30A8 and KCNQ1 along with pharmacokinetic variants in response to sulfonylureas. Method: We performed a prospective study on 209 newly diagnosed subjects; treatment naive T2D subjects were recruited. Individuals were started with glibenclamide monotherapy and followed-up for 12 weeks. Genotyping was done, using PCR-RFLP and TETRA-ARMS PCR and confirmed by DNA sequencing. Results: In univariate regression analysis, KCNJ11 (rs5219) was only the predictor for glibenclamide treatment failure. Conclusion: The present data suggests a possible role of KCNJ11 gene in altered response to glibenclamide.

Original language	English
Pages (from-to)	580-586
Number of pages	7
Journal	Current Molecular Medicine
Volume	17
Issue number	8
DOIs	https://doi.org/10.2174/1566524018666180222122653
Publication status	Published - 01-09-2017

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This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Medicine
Molecular Biology

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10.2174/1566524018666180222122653

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title = "Genetic variants identified from GWAS for predisposition to type 2 diabetes predict sulfonylurea drug response",

abstract = "Background: Several SNPs were identified through GWAS for their association with type 2 diabetes which has implications to pancreatic β-cell physiology. Objective: We aimed to study the role of risk alleles of TCF7L2, KCNJ11, CDKN2A, CDKAL1, IGF2BP2, SLC30A8 and KCNQ1 along with pharmacokinetic variants in response to sulfonylureas. Method: We performed a prospective study on 209 newly diagnosed subjects; treatment naive T2D subjects were recruited. Individuals were started with glibenclamide monotherapy and followed-up for 12 weeks. Genotyping was done, using PCR-RFLP and TETRA-ARMS PCR and confirmed by DNA sequencing. Results: In univariate regression analysis, KCNJ11 (rs5219) was only the predictor for glibenclamide treatment failure. Conclusion: The present data suggests a possible role of KCNJ11 gene in altered response to glibenclamide.",

author = "Phani, \{N. M.\} and M. Vohra and P. Adhikari and Nagri, \{S. K.\} and U. Shashikiran and D{\textquoteright}Souza, \{S. C.\} and Kalluri, \{P. R.R.\} and K. Satyamoorthy and Rai, \{P. S.\}",

year = "2017",

month = sep,

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doi = "10.2174/1566524018666180222122653",

language = "English",

volume = "17",

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journal = "Current Molecular Medicine",

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TY - JOUR

T1 - Genetic variants identified from GWAS for predisposition to type 2 diabetes predict sulfonylurea drug response

AU - Phani, N. M.

AU - Vohra, M.

AU - Adhikari, P.

AU - Nagri, S. K.

AU - Shashikiran, U.

AU - D’Souza, S. C.

AU - Kalluri, P. R.R.

AU - Satyamoorthy, K.

AU - Rai, P. S.

PY - 2017/9/1

Y1 - 2017/9/1

N2 - Background: Several SNPs were identified through GWAS for their association with type 2 diabetes which has implications to pancreatic β-cell physiology. Objective: We aimed to study the role of risk alleles of TCF7L2, KCNJ11, CDKN2A, CDKAL1, IGF2BP2, SLC30A8 and KCNQ1 along with pharmacokinetic variants in response to sulfonylureas. Method: We performed a prospective study on 209 newly diagnosed subjects; treatment naive T2D subjects were recruited. Individuals were started with glibenclamide monotherapy and followed-up for 12 weeks. Genotyping was done, using PCR-RFLP and TETRA-ARMS PCR and confirmed by DNA sequencing. Results: In univariate regression analysis, KCNJ11 (rs5219) was only the predictor for glibenclamide treatment failure. Conclusion: The present data suggests a possible role of KCNJ11 gene in altered response to glibenclamide.

AB - Background: Several SNPs were identified through GWAS for their association with type 2 diabetes which has implications to pancreatic β-cell physiology. Objective: We aimed to study the role of risk alleles of TCF7L2, KCNJ11, CDKN2A, CDKAL1, IGF2BP2, SLC30A8 and KCNQ1 along with pharmacokinetic variants in response to sulfonylureas. Method: We performed a prospective study on 209 newly diagnosed subjects; treatment naive T2D subjects were recruited. Individuals were started with glibenclamide monotherapy and followed-up for 12 weeks. Genotyping was done, using PCR-RFLP and TETRA-ARMS PCR and confirmed by DNA sequencing. Results: In univariate regression analysis, KCNJ11 (rs5219) was only the predictor for glibenclamide treatment failure. Conclusion: The present data suggests a possible role of KCNJ11 gene in altered response to glibenclamide.

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Genetic variants identified from GWAS for predisposition to type 2 diabetes predict sulfonylurea drug response

Abstract

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